<%BANNER%>

Evaluation of Growth Regulating Herbicides for Improved Management of Cogongrass and Torpedograss

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EVALUATION OF GROWTH REGULATING HERBICIDES FOR IMPROVED MANAGEMENT OF COGONGRASS AND TORPEDOGRASS By EILEEN ANN KETTERER A THESIS PRESENTED TO THE GRADUATE SCHOOL OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF SCIENCE UNIVERSITY OF FLORIDA 2007

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2007 Eileen Ann Ketterer 2

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ACKNOWLEDGMENTS I thank my committee chair, Dr. Greg MacDonald, for the countless hours in which he helped me understand my lab and field work as well as making sure that everything was executed smoothly. I thank my committee members Dr. Jay Ferrell, Dr. Ken Boote, and Dr. Brent Sellers for their insight and expertise on my project. Special thanks to all who helped me in the lab and the field, including Justin Snyder, Bob Querns, Danon Moxley, Tim King, Michelle Harmeling, Chris Mudge, Brett Bultimeyer, Jing Jing Wang, Brandon Fast, and Barton Wilder. I thank the Agronomy Department secretaries for their patience and guidance throughout my program. I thank my family and my fianc Jeremy Guest for their continued love and support. Lastly, I thank the Florida Institute of Phosphate Research, the Florida Department of Environmental Protection, the Clanton Black Scholarship Fund, and the Agronomy Department for providing me with the opportunity to research something that I enjoy. 3

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TABLE OF CONTENTS Upage TACKNOWLEDGMENTST...............................................................................................................3 TLIST OF TABLEST..........................................................................................................................6 TABSTRACTT..................................................................................................................................11 1 INTRODUCTIONT...................................................................................................................13 TBiologyT...................................................................................................................................13 CogongrassT......................................................................................................................13 TorpedograssT...................................................................................................................16 TManagementT...........................................................................................................................17 CogongrassT......................................................................................................................17 TorpedograssT...................................................................................................................20 Growth Regulating HerbicidesT........................................................................................22 TRationaleT.................................................................................................................................26 2 INFLUENCE OF GROWTH REGULATOR HERBICIDES ON THE EFFICACY OF GLYPHOSATE AND IMAZAPYR ON COGONGRASS UNDER GREENHOUSE CONDITIONST........................................................................................................................27 TIntroductionT............................................................................................................................27 TMaterials and MethodsT...........................................................................................................29 TDiflufenzopyr Timing StudyT...........................................................................................30 Growth Regulator StudyT.................................................................................................31 TStatistical AnalysisT..........................................................................................................31 TResultsT....................................................................................................................................31 TDiflufenzopyr Timing StudyT...........................................................................................31 Experiment oneT........................................................................................................31 Experiment twoT........................................................................................................33 Growth Regulator StudyT.................................................................................................35 Experiment oneT........................................................................................................35 Experiment twoT........................................................................................................37 TDiscussionT..............................................................................................................................38 3 INFLUENCE OF GROWTH REGULATOR HERBICIDES ON THE EFFICACY OF GLYPHOSATE AND IMAZAPYR ON TORPEDOGRASS UNDER GREENHOUSE CONDITIONST........................................................................................................................46 TIntroductionT............................................................................................................................46 TMaterials and MethodsT...........................................................................................................49 Diflufenzopyr Timing StudyT...........................................................................................49 Growth Regulator StudyT.................................................................................................50 Statistical AnalysisT..........................................................................................................50 4

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TResultsT....................................................................................................................................51 TDiflufenzopyr Timing StudyT...........................................................................................51 TExperiment oneT........................................................................................................51 Experiment twoT........................................................................................................52 Growth Regulator StudyT.................................................................................................53 TExperiment oneT........................................................................................................53 Experiment twoT........................................................................................................54 TDiscussionT..............................................................................................................................55 4 EVALUATION OF GROWTH REGULATOR HERBICIDES FOR IMPROVED CONTROL OF COGONGRASST...........................................................................................64 TIntroductionT............................................................................................................................64 TMaterials and MethodsT...........................................................................................................67 TMethodologyT...................................................................................................................67 TStatistical AnalysisT..........................................................................................................67 TResultsT....................................................................................................................................68 Spring ExperimentT..........................................................................................................68 Summer ExperimentT.......................................................................................................70 Fall ExperimentT...............................................................................................................71 TDiscussionT..............................................................................................................................72 5 EVALUATION OF GROWTH REGULATOR HERBICIDES FOR IMPROVED CONTROL OF TORPEDOGRASST.......................................................................................80 TIntroductionT............................................................................................................................80 TMaterials and MethodsT...........................................................................................................82 MethodologyT...................................................................................................................82 Statistical AnalysisT..........................................................................................................83 TResults and DiscussionT...........................................................................................................83 6 CONCLUSIONST..................................................................................................................86 TLIST OF REFERENCEST..............................................................................................................88 TBIOGRAPHICAL SKETCHT.........................................................................................................97 5

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LIST OF TABLES UTable U Upage U T2-1 Overall model variance for the visual evaluation, shoot regrowth biomass, and rhizome biomass 8 weeks after initial treatment in the cogongrass diflufenzopyr timing Experiment 1.T.........................................................................................................40 T2-2 Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 1.T.................................................................................................................40 T2-3 Cogongrass shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 1.T.................................................................................................................40 T2-4 Cogongrass rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 1.T.................................................................................................................41 T2-5 Overall model variance for the visual evaluation, shoot regrowth biomass, and rhizome biomass 8 weeks after initial treatment in the cogongrass diflufenzopyr timing Experiment 2.T.........................................................................................................41 T2-6 Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 2.T.................................................................................................................41 T2-7 Cogongrass shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings for Experiment 2.T...............................................................................................................42 T2-8 Cogongrass rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings for Experiment 2.T...............................................................................................................42 T2-9 Overall model variance for the visual evaluation, shoot regrowth biomass, and rhizome biomass 8 weeks after initial treatment in the cogongrass growth regulator Experiment 1.T.....................................................................................................................42 T2-10 Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by plant growth regulating herbicides in Experiment 1.T.................................................................................................................43 T2-11 Cogongrass shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by plant growth regulating herbicides in Experiment 1.T.................................................................................................................43 6

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T2-12 Cogongrass rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by plant growth regulating herbicides in Experiment 1.T.................................................................................................................43 T2-13 Overall model variance for the visual evaluation, shoot regrowth biomass, and rhizome biomass 8 weeks after initial treatment in the cogongrass growth regulator Experiment 2.T.....................................................................................................................44 T2-14 Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influences by plant growth regulating herbicides in Experiment 2.T.................................................................................................................44 T2-15 Cogongrass shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influences by plant growth regulating herbicides in Experiment 2.T.................................................................................................................44 T2-16 Cogongrass rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influences by plant growth regulating herbicides in Experiment 2.T.................................................................................................................45 T3-1 Overall model variance for the visual evaluation, shoot regrowth biomass, and rhizome biomass 8 weeks after initial treatment in the torpedograss diflufenzopyr timing Experiment 1.T.........................................................................................................57 T3-2 Percent control of torpedograss regrowth 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 1.T.................................................................................................................58 T3-3 Torpedograss shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 1.T.................................................................................................................58 T3-4 Torpedograss rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 1.T....................................................................................................58 T3-5 Overall model variance for the visual evaluation, shoot regrowth biomass, and rhizome biomass 8 weeks after initial treatment in the torpedograss diflufenzopyr timing Experiment 2.T.........................................................................................................59 T3-6 Percent control of torpedograss regrowth 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 2.T.................................................................................................................59 T3-7 Torpedograss shoot regrowth (grams/pot) 8 weeks after treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 2.T.....................................................................................................................59 7

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T3-8 Torpedograss rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 2.T....................................................................................................60 T3-9 Overall model variance for the visual evaluation, shoot regrowth biomass, and rhizome biomass 8 weeks after initial treatment in the torpedograss growth regulator Experiment 1.T.....................................................................................................................60 T3-10 Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in Experiment 1.T.....................................................................................................................60 T3-11 Torpedograss shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in Experiment 1.T.....................................................................................................................61 T3-12 Torpedograss rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in Experiment 1.T...............................................................................................61 T3-13 Overall model variance for the visual evaluation, shoot regrowth biomass, and rhizome biomass 8 weeks after initial treatment in the torpedograss growth regulator Experiment 2.T.....................................................................................................................62 T3-14 Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in Experiment 2.T.....................................................................................................................62 T3-15 Torpedograss shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in Experiment 2.T.....................................................................................................................63 T3-16 Torpedograss rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in Experiment 2.T...............................................................................................63 T4-1 Overall model variance for the control evaluations 3, 6, and 9 months after treatment (MAT) in the cogongrass spring field experiment.T...........................................................74 T4-2 Averaged across plant growth regulating herbicides, the effect of herbicide and month of application on cogongrass control 3 months after initial plant growth regulating herbicide application for the spring experiment.T..............................................75 T4-3 Averaged across herbicides, the effect of plant growth regulating herbicide and month of application on cogongrass control 3 months after initial plant growth regulating herbicide application for the spring experiment.T..............................................75 8

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T4-4 Averaged across plant growth regulating herbicides, the effect of herbicide and month of application on cogongrass control 6 months after initial plant growth regulating herbicide application for the spring experiment.T..............................................75 T4-5 Averaged across month of application, the effect of herbicide and growth regulator on cogongrass control 6 months after initial plant growth regulating herbicide application for the spring experiment.T...............................................................................76 T4-6 Averaged across herbicide, the effect of growth regulator and month of application on cogongrass control 6 months after initial plant growth regulating herbicide application for the spring experiment.T...............................................................................76 T4-7 Averaged across plant growth regulating herbicide, the effect of growth regulator and month of application on cogongrass control 9 months after initial plant growth regulating herbicide application for the spring experiment.T..............................................76 T4-8 Averaged across month of application, the effect of growth regulator and herbicide on cogongrass control 9 months after initial plant growth regulating herbicide application for the spring experiment.T...............................................................................76 T4-9 Averaged across herbicides, the effect of growth regulator and month of application on cogongrass control 9 months after initial plant growth regulating herbicide application for the spring experiment.T...............................................................................77 T4-10 Overall model variance for the control evaluations 3 and 6 months after treatment (MAT) in the cogongrass summer field experiment.T.........................................................77 T4-11 Effect of growth regulator, averaged across herbicide and month of glyphosate or imazapyr application, on cogongrass control 3 months after initial plant growth regulating herbicide application for the summer experiment.T...........................................77 T4-12 Effect of month of application, averaged across herbicide and plant growth regulating herbicides, on cogongrass control 3 months after initial plant growth regulating herbicide application for the summer experiment.T...........................................78 T4-13 Averaged across plant growth regulating herbicides, the effect of herbicide and month of application on cogongrass control 6 months after initial plant growth regulating herbicide application for the summer experiment.T...........................................78 T4-14 Effect of growth regulator, averaged across herbicide and month of glyphosate or imazapyr application, on cogongrass control 6 months after initial plant growth regulating herbicide application for the summer experiment.T...........................................78 T4-15 Overall model variance for the control evaluation 3 months after treatment (MAT) in the cogongrass fall field experiment.T.................................................................................78 9

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T4-16 Effect of growth regulator, averaged across herbicide and month of glyphosate or imazapyr application, on cogongrass control 3 months after initial plant growth regulating herbicide application for the fall experiment.T...................................................79 T4-17 Effect of month of application, averaged across herbicide and plant growth regulating herbicide, on cogongrass control 3 months after initial plant growth regulating herbicide application for the fall experiment.T...................................................79 T5-1 Overall model variance for the control evaluations 3 and 6 months after treatment (MAT) in the torpedograss field experiment.T....................................................................84 T5-2 Influence of plant growth regulating herbicides applied with glyphosate and imazapyr for control of torpedograss at 3, 6, and 9 months after treatment (MAT).T........85 10

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Abstract of Thesis Presented to the Graduate School of the University of Florida in Partial Fulfillment of the Requirements for the Degree of Master of Science EVALUATION OF GROWTH REGULATING HERBICIDES FOR IMPROVED MANAGEMENT OF COGONGRASS AND TORPEDOGRASS By Eileen Ann Ketterer May 2007 Chair: Gregory E. MacDonald Major: Agronomy Cogongrass [Imperata cylindrica (L.) Beauv.] and torpedograss (Panicum repens L.) are invasive perennial grasses in Florida that cannot effectively be controlled to the point of complete eradication without intense and often unfeasible means. The biggest hurdle in developing a long-term management strategy for cogongrass and torpedograss is rhizome control. Large rhizome to foliage ratio allows the plants to store photosynthates in the rhizomes. Cogongrass rhizomes exhibit a form of apical dominance which suppresses the growth of shoots from subapical nodes. Torpedograss, though lacking apical dominance, is primarily found in seasonally wet or submerged aquatic settings. Herbicide efficacy on torpedograss usually correlates with the proportion of emergent stems to the amount of herbicide interception at a given rate. It is hypothesized that disruption of normal auxin levels in torpedograss and cogongrass would encourage new secondary shoot production. We sought to achieve abnormal auxin levels using plant growth regulating (PGR) herbicides and follow this with different rates and application timings of glyphosate or imazapyr to improve efficacy. Both greenhouse and field studies were conducted using glyphosate and imazapyr combined in various treatments with the PGR herbicides 2,4-D, dicamba, diflufenzopyr, quinclorac, and triclopyr. Greenhouse treatments were separated into 2 studies. The first study 11

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examined the effect of diflufenzopyr timing (0.22 kg-ai/ha). Either no diflufenzopyr was applied, or it was applied either 3 days before, tank-mixed with, or 3 days after glyphosate or imazapyr treatments. Glyphosate rates included 0.0, 0.43, 0.84, and 1.68 kg-ai/ha, while imazapyr rates included 0.0, 0.14, 0.28, and 0.56 kg-ai/ha. The second study examined PGR herbicides (2,4-D 1.12 kg-ai/ha, dicamba 0.56 kg-ai/ha, triclopyr 0.56 kg-ai/ha, and quinclorac 1.40 kg-ai/ha) tank mixed with either glyphosate or imazapyr with the same rates as the diflufenzopyr study. The field studies examined whether shoot stimulation from PGR herbicides (2,4-D 1.12 kg-ai/ha, dicamba 0.56 kg-ai/ha, diflufenzopyr 0.28 kg-ai/ha, triclopyr 0.42 kg-ai/ha, and quinclorac 1.40 kg-ai/ha) would result in better glyphosate or imazapyr efficacy (3.36 and 0.84 kg-ai/ha, respectively). Torpedograss treatments were all tank-mixed and applied the same day, while glyphosate or imazapyr treatments for cogongrass were applied once, on the same day (0 month) or 1, 2, or 3 months after the initial PGR herbicide application. Results from these experiments indicate that PGR herbicides provide varied levels of control when used with glyphosate or imazapyr. In the greenhouse, consistent cogongrass control came from imazapyr tank-mixed with diflufenzopyr or 2,4-D (> 80% control, after 8 weeks with 0.56 kg-ai/ha of imazapyr). Torpedograss greenhouse results indicated no consistent trend in control. In the field, cogongrass was best controlled when imazapyr was applied with any PGR herbicide, at any of the tested intervals, providing approximately 85% control or greater. When glyphosate was applied to cogongrass 2 or 3 months after PGR herbicides, > 80% control was observed at 6 and 9 months. Most PGR herbicides had no effect on glyphosate or imazapyr efficacy for torpedograss. Overall, it appears that cogongrass control can be improved if treated with PGR herbicides, while torpedograss requires more research. 12

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CHAPTER 1 INTRODUCTION Cogongrass [Imperata cylindrica (L.) Beauv.] and torpedograss (Panicum repens L.) are invasive perennial grasses (Dickens 1974, Holm et al. 1977, Wilcut et al. 1988b). Both of these plants appear on multiple state noxious weed lists, with cogongrass also appearing on the federal list (USDA 2005a, 2005b). While there is abundant literature on the control of cogongrass (MacDonald 2004) and limited information on torpedograss (Sartain 2003), neither plant can be effectively managed to the point of complete eradication without great and often unfeasible means (Willard et al. 1997, Willard et al. 1998, Smith et al. 1999). Biology Cogongrass Cogongrass is a cosmopolitan species that has been reported on every continent except Antarctica (Coile and Shilling 1993), and currently infests over 500 million ha worldwide (Dickens 1974, Holm et al. 1977, Flavey 1981). At least seventy-three countries report problems with cogongrass in agricultural fields, pastures, and roadside settings (Holm et al. 1977). It is also problematic in natural areas where it displaces native vegetation (Shilling 1996). Introduction of cogongrass into the United States occurred around 1911 in Mobile, Alabama, from packing material shipped from Japan (Tabor 1949). Cogongrass was also intentionally introduced from the Philippines as a potential forage at McNeil Mississippi Agricultural Station (Hubbard et al. 1944, Tabor 1949, Dickens and Buchanan 1975). Cogongrass tends to invade disturbed areas with high sunlight, such as reclaimed mines, pine plantations, pastures, rangelands, and natural areas (Willard et al. 1990, Coile and Shilling 1993, Shilling 1996). Canopy closure and shade appear to deter cogongrass establishment (Soerjani 1970). Although not considered a shade species, studies have shown that cogongrass 13

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adapts to shade via increases in leaf area, leaf weight ratio, and leaf area ratio (Patterson et al. 1980). Several light compensation studies also showed that cogongrass has a low compensation point in relation to most plants (32 to 35 mol mP-2P sP-1P) indicating survival even in highly competitive and light limiting environments (Gaffney 1996, Jose et al. 2002). Cogongrass exhibits many features that allow it to be highly competitive. The silica bodies on the edge of mature leaves deter herbivory (Coile and Shilling 1993). This, coupled with poor quality, makes it unpalatable and unsuitable as a forage crop (Coile and Shilling 1993). The pyrogenic nature of cogongrass also contributes to its success as a weed (Patterson et al. 1980). Dead cogongrass leaves do not detach and decompose, but remain on the plant and become highly flammable when desiccated (Coile and Shilling 1993). Although many native grasses in the southeastern United States are adapted to fire ecology, the fires that occur in cogongrass communities are hotter and more intense, resulting in the displacement of native vegetation (Lippincott 2000, Rossiter et al. 2003). Studies have also shown that cogongrass exudes allelopathic compounds from both foliage and roots (Koger and Bryson 2003) which deter the vegetative growth of specific plants near existing or recently removed stands of cogongrass (Inderjit and Dakshini 1991, Hussain et al. 1992, Johnson et al. 1997, Koger and Bryson 2003). This allelopathy has also been shown to suppress germination and seedling growth of certain crops (Inderjit and Dakshini 1991, Koger and Bryson 2003). This plant has the ability to invade, not only on disturbed areas, but also in vegetatively intact communities via seeds (King and Grace 2000). Cogongrass produces over 3000 seeds per plant (Holm et al. 1977) of which 80 to 90% are viable (Shilling et al. 1997). However, optimum seed germination occurs immediately after seed set and rapidly declines after 3 months with almost complete loss of viability after one year (Shilling et al. 1997). Viable cogongrass seeds 14

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are reported to be only produced through out-crossing (Gabel 1982, McDonald et al. 1996). There are conflicting reports regarding cogongrass seed dispersal in Florida. Willard and Shilling (1990) suggested that rhizomes were solely responsible for cogongrass spread. This theory was supported by McDonald et al. (1996) who did not detect out-crossing in Florida. However, Shilling et al. (1997) did collect viable seeds, suggesting that out-crossing occurs or a different population has developed in this area since the results from the 1990 study by Willard et al. (1990). Cogongrass rhizomes begin to form soon after seed germination or rhizome sprouting (Ayeni 1985). Eussen (1979) reported eleven weeks after initial rhizome growth, the rhizome mass may occupy an area as large as 4mP2P. In a mature stand, cogongrass can develop as many as 350 shoots from its rhizome mass in a 6-week period (Eussen 1979). A mature and densely populated stand of cogongrass can have rhizomes weighing as much as 40 tons fresh weight per hectare (Terry et al. 1997, English 1998). Rhizomes comprise greater than 60% of total biomass (Sajise 1976) and Terry et al. (1997) suggested that cogongrass may even sacrifice leaf production to maintain this high ratio (Sajise 1972, Sajise 1976). As it grows, the rhizomes branch out in many directions, forming a dense rhizomatous mat. This mat excludes vegetative roots or rhizomes of other species from becoming established within a cogongrass stand (Dozier et al. 1998). Cogongrass rhizomes are very resistant to high temperatures and fire has been hypothesized to stimulate dormant rhizome buds, promoting larger, denser cogongrass stands (Coile and Shilling 1993). Rhizomes have an incredible regeneration capacity and this capacity is positively correlated with increased weight, height, age, length, thickness of rhizomes, and visible buds (Ayeni 1985). Regeneration cannot occur with newly formed rhizomes as they lack roots and 15

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therefore the ability to take up nutrients (Ayeni 1985, Ayeni and Duke 1985). Success of rhizome regeneration also depends upon depth of burial (Lee 1977, Wilcut et al. 1988a), the location of the rhizome segment on the original rhizome, and the proximity to the apical buds (Holm et al. 1977, Gaffney 1996, Wilcut et al. 1988a, English 1998). Torpedograss Torpedograss is an old world Eurasian plant (Holm et al. 1977). Although the exact reason for introduction is unknown, it is speculated that torpedograss either came to the Southeastern United States via ship ballasts or was introduced as a potential wetland forage (Tabor 1952). In the United States, torpedograss is found from Florida to Texas (Wilcut et al. 1988a, McCarty et al. 1993). This plant is most frequently found near or in aquatic sites (Holm et al. 1977) and Florida Department of Environmental Protection ranks torpedograss as the 2PndP most abundant plant in Florida lakes (Schardt 1992, Schardt personal communication, February 2007). It can also be found on terrestrial areas such as golf courses and roadsides (Brecke and Unruh 2001). The presence of torpedograss is problematic in Florida because it interrupts flood control, irrigation and turf production (Shilling and Haller 1989, McCarty et al.1993). While torpedograss produces seeds, reports suggest these seeds may be non-viable and the primary means of reproduction is through rhizomes (Wilcut et al. 1988a, Ferriter et al. 2006). However, viability and spread from seed has been reported in Portugal (Peng 1984). Similar to cogongrass, torpedograss rhizomes comprise approximately 70 to 90% of the total biomass (Smith et al. 1999). This plant also has a very high rhizome regeneration rate (92 to 96% of rhizome buds at 20 to 35C) from small segments (Hossain et al. 2001). Torpedograss produces new buds along the entire length of the rhizome contributing to the dense rhizome mass (Wilcut et al. 1988a). 16

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Management Complete control of cogongrass and torpedograss requires total removal of all viable tillers and rhizomes (Tanner et al. 1992, Willard et al. 1997, Smith et al. 1999). There have been numerous studies to identify best management practices for the control of these plants, but none have yielded 100% control longer than 24 months within time constraints and budgets (Willard et al. 1997, Willard et al. 1998, Smith et al. 1999). Another issue in natural areas is that lands are set aside for conservation of the native plant community (Langeland and Stocker 2001). There is a need for management in these natural areas that will not damage desirable, non-target species (Halpin 1997, Langeland and Stocker 2001). Since both cogongrass and torpedograss occur in natural areas, management strategies employing mechanical or cultural methods may not be practical. Cogongrass Biological control for cogongrass has been disappointing with very few, if any, organisms providing appreciable control (Soerjani 1970, Coile and Shilling 1993). Recent studies indicate a host of organisms are found on this plant, including fungi, insects, nematodes, mites and one parasitic plant (Minno and Minno 1999, Minno and Minno 2000). While there is still a chance that one or more of these organisms could be used as a control, there is no conclusive evidence that would suggest any successful biological control agents. Biological control studies are currently being conducted in conjunction with other control methods (Yandoc et al. 2004, Yandoc et al. 2005). There have been a number of studies that utilize cover crops as a cultural technique to control cogongrass (Menz and Grist 1996, Otsamo et al. 1997, Akobundu et al. 2000, Versteeg and Koudokpon 1990). This approach suggests that landholders consider long-term management involving the use of other crops to crowd out cogongrass (MacDonald 2004). Crops can include 17

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legumes such as velvetbean (Mucuna pruriens var. utilis) (Versteeg and Koudokpon 1990, Akobundu et al. 2000), and rubber trees (Hevea brasiliensis) (Menz and Grist 1996), as well as other species. These crops can slow and reduce cogongrass growth in as few as 2 to 5 years (Akobundu et al. 2000). Studies have also included the use of other exotic tree species that are fast growing and quick to shade out and suppress cogongrass (Otsamo et al. 1997). Others have also shown cogongrass seedlings to be suppressed by greater than 75% with bahiagrass cover (Willard and Shilling 1990, Shilling et al. 1997). While these techniques may be beneficial in agricultural settings, these methods cannot be utilized in natural areas where the preservation of desirable species is a priority in addition to controlling cogongrass (Langeland and Stocker 2001). Mechanical approaches such as discing, mowing, and fire to control cogongrass have had mixed results (Wilcut et al. 1988a, Coile and Shilling 1993, McCarty et al. 1993, Lippincott 1997). Studies have shown that cogongrass cannot survive in heavily cultivated areas (Coile and Shilling 1993). Deep tilling during the dry season exhausts the food supply by drying out rhizomes (Soerjani 1970, Johnson et al. 1997), and burying the rhizomes to a depth where growth of new shoots is less likely, > 8cm (Ivens 1980, Wilcut et al. 1988a). Deep and repeated tillage breaks apical dominance, promoting shoot growth, thus increasing the amount of herbicide that is absorbed in chemical applications (Willard et al. 1996). However, frequency of tilling is an important factor in controlling cogongrass, as Johnson et al. (1999) reported that infrequent cogongrass discing may be ineffective and might promote the species. Mechanical control is not always an option for control in natural areas as the soil disturbance and heavy equipment may provide more damage than benefit (Langeland and Stocker 2001). 18

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The use of fire has been considered and implemented for cogongrass control, but thus far, it only seems to promote cogongrass (Lippincott 1997). Fire temperatures, duration, and intensities are well below what is needed to desiccate cogongrass rhizomes (Holm et al. 1977, Soerjani 1970). Unless cogongrass rhizomes can be directly burned after mechanical control has been utilized, this is not an effective control option. A number of chemical control studies have been performed on cogongrass (Dickens and Buchanan 1975, Baird et al. 1983, Bacon 1986, Lee 1986, Tanner et al.1992). Herbicide applications to cogongrass are difficult due to the level of dead leaves preventing total herbicide coverage (Coile and Shilling 1993). Studies involving graminicides (grass specific herbicides) have shown that these chemicals have little effect on cogongrass (Mask et al. 2000). Those herbicides having the best results include glyphosate N-(phosphonomethyl)glycine, imazapyr 2-[4,5-dihydro-4-methyl-4-(1-methylethyl)-5-oxo-1-H-imidazol-2-yl]-3-pyridinecarboxylic acid, and dalapon (2,2-Dichloropropionic acid, no longer registered) (Willard et al. 1997). Glyphosate produces rapid cogongrass defoliation (Townsend and Butler 1990) with no soil residual activity (WSSA 2002). Young cogongrass leaves, possibly due to less developed cuticles, are most susceptible to glyphosate treatment (Lee 1986). A thicker cuticle would help prevent the entry of harmful substances (e.g., too much sunlight or herbicides) (Wanamarta and Penner 1989). Imazapyr is slower acting, but provides better long term control due to residual soil activity (Johnson et al. 1997, Willard et al. 1997). There have been several reports that herbicide applications in the fall provide increased control with glyphosate or imazapyr (Gaffney 1996, Johnson et al. 1999). Johnson et al. (1997) reported imazapyr (0.84 kg-ai/ha) and glyphosate (2.24 kg-ai/ha) provided 70 to 80% control up to 1 year after treatment when applied in the fall. Gaffney (1996) also indicated > 20% more 19

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control was achieved 1 year after treatment with the same herbicides and rates in a fall application versus a spring or summer application. Torpedograss Very little biological control research has been done on torpedograss due to the reluctance to use this method on grasses in general (Bodle and Hanlon 2001). Chandramohan et al. (2003) indicated that three native fungi (Drechslera gigantea, Exserohilum longirostratum, and E. rostratum) may manage torpedograss for 7 to 9 months. The option of biological control is expanding but more research is needed in this area. Mechanical techniques do not have the same effect on torpedograss as with cogongrass. Instead, torpedograss is actually promoted by cultivation, as any fragmentation of the rhizomes can result in a large amount of new plants in a short amount of time after a 4 week lag phase (Holm et al. 1977, Wilcut et al. 1988a, Sutton 1996,). Even simple maintenance techniques such as core aeration have been shown to increase torpedograss density in turf (McCarty et al. 1993). The invasion of torpedograss is due, in part, to a lack of strong apical dominance in rhizomes as well as high rhizome regeneration rate (similar to cogongrass) and an increased ability to store water and nutrients in times of stress (Wilcut et al. 1988a). As with cogongrass, torpedograss is not adversely affected by burning alone (Hanlon and Langeland 2000). However, it appears that the best form of torpedograss control occurs when herbicide application follows a burn. In a study by Hanlon and Langeland (2000) there was little long term control of torpedograss if it was not burned prior to herbicide treatment. When evaluated 42 weeks after treatment, imazapyr applied 6 weeks after a burn provided 65 to 85% control, compared to < 20% when applied to non-burned plants. There have been several herbicide control studies on torpedograss but the herbicides glyphosate and imazapyr provide the most acceptable control (Baird et al. 1983, Shilling and 20

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Haller 1989, Willard et al. 1998, Smith et al. 1999, Hanlon and Langeland 2000). Both herbicides are broad-spectrum herbicides. However, glyphosate has little to no soil residual activity, whereas the residual activity of imazapyr is high due to its long soil half-life, 25 to 142 days (WSSA 2002). Limited control from glyphosate is often attributed to the aquatic habitat of torpedograss. When the plant is treated under such conditions, the herbicide only reaches the emergent portion (Smith et al. 1999). Studies show that this portion of the plant usually dies but regrowth from rhizomes and submerged stems segments often occurred within a few months (Baird et al. 1983). Smith et al. (1999) concluded that high water levels inhibit foliar interception of glyphosate and control correlated with foliar exposure to water level ratio. To achieve 90% control (5 weeks after initial treatment), a glyphosate application rate of 2.24 kg-ai/ha was needed to be intercepted by at least 40% of the foliage. Lower rates correlated with a higher percentage of foliage cover to achieve similar results (Smith et al. 1999). Imazapyr applications on torpedograss have produced similar problems with submergence and in turn, less control (Hanlon and Langeland 2000). Inconsistencies in data presented by Hanlon and Langeland (2000) lead the authors to speculate that fluctuating water depth at different experimental sites could have influenced results. While all experiments began in approximately 0.8 meters of water, by the end of the experiment, one study site was considered dry while the remaining sites were flooded. Greater than 95% control was observed at the dry site with < 25% control at the flooded sites. The authors also speculated that thatch levels may have contributed to inconsistent control. The amount of torpedograss tissue exposed to the herbicide may be reduced as thatch increased (Hanlon and Langeland 2000). 21

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Growth Regulating Herbicides As previously mentioned, both cogongrass and torpedograss have a high rhizome to shoot ratio, contributing to their success (Sajise 1976, Smith et al. 1999). Having a high rhizome:shoot ratio allows for the build up of carbohydrate reserves. These reserves have long been thought to mobilize when photosynthetic material is reduced, such as defoliation through herbicide application or other means (White 1973, Deregibus et al. 1982). However, other studies have shown that plant growth may be the result of activating molecules as well as carbohydrate reserves and may involve bud activation (Watson and Casper 1984, Richards and Caldwell 1985). When buds are suppressed, carbohydrate reserves accumulate (White 1973). Bud suppression is mostly due to plant hormones such as auxins or cytokinins (Cline 1997). Cytokinins work to stimulate cell division (Taiz and Zeiger 2006). When lateral rhizome buds are formed cytokinins are promoted at the site (Cline 1997). Once the rhizomes form the apexes, then auxins are released (Cline 1997). These auxins will suppress buds growing below the apex (Cline 1997, Taiz and Zeiger 2006). The level of apical dominance exhibited in a plant depends upon the level of auxins present in the apex (Cline 1997). The ratio of auxins to cytokinins determines whether rhizome production or shoot production will increase. A high auxin:cytokinin ratio equates to more root/rhizome production, whereas a low ratio causes more shoot production (Taiz and Zeiger 2006). In the event of a physical removal of a rhizomatous apex, cytokinins are released and auxin decreases (Cline 1997). Subapical buds begin to grow as the auxin:cytokinin ratio decreases (Taiz and Zeiger 2006). Once these subapical buds begin to grow, auxins and gibberellins are then promoted again (Cline 1997). Gibberellins stimulate shoot production (Taiz and Zeiger 2006). Plant growth regulating herbicides (PGR herbicides) are widely used for weed control (Sprecher and Stewart 1995, Ketchersid and Senseman 1998, Grossman et al. 2002, Lym and 22

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Deibert 2005). Diflufenzopyr [2-(1-[([3,5-difluorophenylamino]carbonyl)-hydrazono]ethyl)-3-pyridinecarboxylic acid], triclopyr [(3,5,6-trichloro-2-pyridinyl)oxy], picloram (4-amino-3,5,6-trichloro-2-pyridinecarboxylic acid), clorpyralid (3,6-dichloro-pyridine carboxylic acid), quinclorac (3,7-Dichloro-8-quinolinecarboxylic acid), dicamba (3,6-dichloro-2-methoxybenzoic acid), and 2,4-D [(2,4-dichlorophenoxy) acetic acid] are commonly used PGR herbicides (Anderson 1996, Ketchersid and Senseman 1998, Grossman et al. 2002). Herbicides in this classification interfere with growth hormone functions and have similar modes of action and selectivity (Anderson 1996). While the true mode of action of some of these herbicides is unknown, it is speculated that some of these PGR herbicides have auxin-like properties which mimic auxins in an unregulated fashion (e.g., 2,4-D, dicamba, diflufenzopyr, quinclorac) (WSSA 2002). Other growth regulating herbicides such as diflufenzopyr inhibit the transport of auxins (Grossman et al. 2002, WSSA 2002). By mimicking or interfering with auxins, PGR herbicides interfere with nucleic acid metabolism, and upset normal hormone balance, cell enlargement, protein synthesis, and even respiration (Anderson 1996). Auxin-like compounds have been used in agriculture and horticulture for years to promote growth for desirable species (Basra 2000). Sugarcane (Saccharum spp. hybrids) is an example of a crop that uses auxin-like compounds to increase regeneration rate for vegetatively propagated plants as necessitated by the high demand for genetically uniform sugarcane products in consumer diets (Franklin et al. 2006). Diflufenzopyr in conjunction with the herbicide dicamba has been studied as an option in controlling broadleaf invasive plants (Grossman et al. 2002). Studies involving the invasive broadleaf plants leafy spurge (Euphorbia esula L.) and Canada thistle (Cirsium arvense L.), showed the combination of diflufenzopyr and dicamba provided superior control compared to either herbicide alone (Lym and Deibert 2005). 23

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Application timing of diflufenzopyr appears to be critical for control (Ketchersid and Senseman 1998). The combination of diflufenzopyr and dicamba proved more phytotoxic to other broadleaves such as field bindweed (Convovulus arvense L.) and velvetleaf (Abutilon theophrasti Medic.) when diflufenzopyr was applied 3 days before the herbicide compared to diflufenzopyr in conjunction with or after application (Ketchersid and Senseman 1998). Broadleaf plants can be controlled efficiently with diflufenzopyr (Lym and Deibert 2005), but little is known about diflufenzopyr in grasses, specifically invasive perennial grasses. Triclopyr is primarily used to control woody and broadleaf species (WSSA 2002). There is either limited information or lack of positive results for the use of triclopyr in invasive grasses (WSSA 2002). In aquatic studies, this herbicide has high selectivity for certain invasive species while causing little damage to native plants, such as Eurasian watermilfoil (Myriophyllum spicatum L.) (Sprecher and Stewart 1995). 2,4-D and dicamba are both speculated to be auxin mimics. These two herbicides along with triclopyr increase the evolution of ethylene which produces uncontrolled growth known as epinasty (WSSA 2002). 2,4-D is a long standing herbicide which has primarily been used in broad situations from agriculture and pastures, to aquatics (WSSA 2002). While this herbicide has been reported to have little or no activity on grasses, it does control a wide range of broadleaf weeds (WSSA 2002). Dicamba can be applied as a PRE or POST emergence application. It is used on pastures, turf, and some row crops (WSSA 2002). Unlike 2,4-D this herbicide does have some activity on grasses as well as many broadleaf weeds such as Canada thistle (WSSA 2002). While there are limited data on the effects of quinclorac on cogongrass, torpedograss is moderately susceptible to this herbicide (Anonymous 2006). Quinclorac is labeled for torpedograss control in bermudagrass (Cynodon dactylon) (Anonymous 2006). However, 24

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multiple applications are necessary to achieve acceptable control. McCarty et al. (1993) concluded that multiple quinclorac applications at 2.2 kg-ai/ha followed by 1.1 kg-ai/ha 3 and 6 weeks after initial treatment (WAT) could control torpedograss (85 to 90% control) for 7 to 10 WAT. Busey (2003) found 4 applications at 0.42 kg-ai/ha a year for 2 years reduced torpedograss dry weight 80%. While absorption and translocation of quinclorac occur in both the foliage and the roots, it is more often absorbed and translocated through the roots of torpedograss (Williams et al. 2004). A study by Williams et al. (2004) indicated that at 4 WAT the fresh weight foliage of torpedograss was reduced 39% regardless of rate (0.56, 0.78, 1.01, and 1.23 kg-ai/ha) when quinclorac was applied directly to the soil, compared to soil and foliar application and foliar application alone (36 and 21% respectively). However, at 7 WAT, foliage was reduced 74% with the foliar and soil combined application of quinclorac compared to foliar and soil applications alone (25 and 40% reduction, respectively). At 10 WAT, foliage reduction was highest with the foliar application alone (26%) and soil application alone had the least foliage reduction (2%). Williams et al. (2004) speculated that soil-applied quinclorac may have leached out of the rooting zone indicating that there could be adverse effects of quinclorac if applied to torpedograss in a submersed area (Williams et al. 2004). Although seeds are a concern with cogongrass, the biggest hurdle in developing a viable management strategy for cogongrass and torpedograss is control of rhizomes. While apical dominance is weak in torpedograss rhizomes, cogongrass rhizomes exhibit a strong form of apical dominance which suppresses the growth of shoots from subapical nodes (Wilcut et al. 1988a, Cline 1994, Gaffney and Shilling 1995). Gaffney (1996) reported that cogongrass rhizomes with apices removed produced 31% more shoots than rhizomes with intact apices. 25

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Therefore, disruption of normal auxin levels in rhizome grasses could encourage new shoot production of otherwise dormant buds (Cline 1994, English 1998). This generally occurs with physical injury, but it has been hypothesized that plant growth regulator herbicides could cause this effect as well. As for torpedograss, rhizome manipulation may result in increased emergent shoots. This too may be achieved using PGR herbicides. Since cogongrass and torpedograss occur in areas that preclude mechanical disturbance, the use of growth regulating herbicides in conjunction with current control methods warrants research. Rationale Herbicide treatments often do not provide complete control of cogongrass or torpedograss, although field observations have shown increased levels of control with different combinations of growth regulating herbicides. We hypothesize that herbicides are unequally distributed among meristematic regions in the rhizomes, perhaps because of apical dominance in cogongrass or the aquatic habitat of torpedograss. These studies will address the hypothesis that the combination of plant growth regulating herbicides with glyphosate or imazapyr will increase herbicide efficacy in cogongrass and torpedograss by providing more complete distribution of herbicides. The specific objectives follow: Determine the effect of diflufenzopyr application timing on the efficacy of glyphosate and imazapyr on cogongrass and torpedograss under greenhouse conditions Determine the effect of growth regulating herbicides on the efficacy of glyphosate and imazapyr on cogongrass and torpedograss under greenhouse conditions Determine the impact of growth regulating herbicides on the control of cogongrass and torpedograss with glyphosate or imazapyr under field conditions 26

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CHAPTER 2 THE INFLUENCE OF GROWTH REGULATOR HERBICIDES ON THE EFFICACY OF GLYPHOSATE AND IMAZAPYR ON COGONGRASS UNDER GREENHOUSE CONDITIONS Introduction Cogongrass [Imperata cylindrica (L.) Beauv.], an invasive perennial grass, is considered noxious by both state and federal agencies (Dickens 1974, Holm et al. 1977, USDA 2005a, 2005b). While there is abundant literature on the control of cogongrass (MacDonald 2004), these reports indicate that sustaining high levels of control cannot be accomplished without intense and often unfeasible means (Willard et al. 1997). For example, landowner can expect to pay greater than $200/ha per year for chemical control alone (Ramsey et al. 2003, as cited in Matta and Alavalapati 2007). Even with this level of expense, only 2 to 3 years of 40 to 60% control, at most, will be observed (Willard et al. 1996, Willard et al. 1997). A number of herbicidal studies have been performed on cogongrass (Dickens and Buchanan 1975, Baird et al. 1983, Bacon 1986, Lee 1986, Tanner et al. 1992, Barnett et al. 2001). Those herbicides having the best results are limited to glyphosate N-(phosphonomethyl) glycine and imazapyr 2-[4,5-dihydro-4-methyl-4-(1-methylethyl)-5-oxo-1-H-imidazol-2-yl]-3-pyridinecarboxylic acid (Willard et al. 1997). Willard et al. (1996) reported that glyphosate and imazapyr provide roughly 40 to 60% control on cogongrass 2 years after treatment. Glyphosate produces almost immediate cogongrass defoliation, with no soil residual activity (Townsend and Butler 1990). Imazapyr is slower acting, but provides better long term control due to residual soil activity (Johnson et al. 1997, Willard et al. 1997). Applications of 3.4 kg-ai/ha of glyphosate and 0.8 kg-ai/ha of imazapyr provided 60 and 70% control of regrowth 19 months after initial treatment, respectively, when applied alone (Willard et al. 1997). However, when glyphosate and 27

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imazapyr were sequentially applied, control ranged from 87 to 98% 19 months after initial treatment regardless of application order (Willard et al. 1997). One of the major reasons that cogongrass is such a successful invader is due to its extensive rhizome system. Rhizomes comprise greater than 60% of the entire plants biomass (Sajise 1976). Eussen (1979) reported eleven weeks after initial rhizome growth, the rhizome mass may occupy an area as large as 4mP2P. In a mature stand, cogongrass can develop as many as 350 shoots from its rhizome mass in a 6-week period (Eussen 1979). Rhizomes can produce as much as 40 tons fresh weight per ha in dense stands (Terry et al. 1997, English 1998). Rhizomes exhibit a form of apical dominance which suppresses the growth of shoots from subapical nodes (Cline 1994). Due to its extensive rhizome network, all viable tillers and rhizomes of cogongrass must be controlled to prevent regrowth (Tanner et al. 1992, Willard et al. 1997). Numerous studies involving biological, mechanical, cultural, and chemical control have indicated that the most consistent and effective method for cogongrass control is through herbicide application. However, the best management practices for cogongrass, regardless of method or integration of methods have not yielded 100% long term control (> 24 months) within time constraints and budgets for the average landowner (Willard et al. 1997). Poor, long term herbicide control may be the result of apical dominance, possibly causing unequal distribution of carbohydrates and, consequently, systemic herbicides in the rhizomes. Studies on auxins suggest that these hormones play a role in apical dominance in cogongrass (Gaffney and Shilling 1995). Gaffney (1996) reported that cogongrass rhizomes with apices removed produced 31% more shoots than rhizomes with intact apices. Therefore, disruption of normal auxin levels in cogongrass could encourage new shoot production of otherwise dormant 28

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buds (Cline 1994, English 1998). This generally occurs with physical injury, but it has been hypothesized that plant growth regulating herbicides (PGR herbicides) could cause this effect as well. By disrupting apical dominance, systemic herbicides may be distributed more evenly and potentially provide more complete control. There are several herbicides that interfere with normal auxin function in plants. These include triclopyr, 2,4-D, dicamba, quinclorac, and diflufenzopyr (WSSA 2002). It is speculated that some of these PGR herbicides have auxin-like properties that mimic auxins in an unregulated fashion with plants, while others block the transport of auxins (Anderson 1996, WSSA 2002, Lym and Deibert 2005). Previous research by English (1998) studied the impact of some growth regulating herbicides on bud break in cogongrass and found that diflufenzopyr increased sprouting in 21% of previously dormant buds, using a 0.5 ppm concentration. Other growth regulating herbicides such as 2,4-D resulted in < 10% bud break at 5 ppm and did not differ from untreated plants. Since cogongrass occurs in areas that preclude mechanical disturbance, the use of growth regulating herbicides in conjunction with current control methods warrants research. The application timing of diflufenzopyr and the combination of glyphosate or imazapyr with growth regulating herbicides has never been studied on cogongrass. Thus, this study has two objectives: 1.) determine the effect of diflufenzopyr application timing on the efficacy of glyphosate and imazapyr on cogongrass, and 2.) determine the effect of growth regulating herbicides, other than diflufenzopyr, on the efficacy of glyphosate and imazapyr on cogongrass. Materials and Methods Cogongrass plants were established from rhizomes that were obtained from local Gainesville populations. Plants were grown under greenhouse conditions with the following 29

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environmental parameters: 12 hr day, 12 hr night, temperature 30/20C. Cogongrass was grown in 3L pots with commercial potting soilTP1PT and amended with slow-release fertilizerTP2PT. Plants were grown for 8 to 10 weeks to ensure a dense and healthy rhizome mass. Treatments for both studies were applied using a standard small plot sprayer with appropriate nonionic surfactant (0.25% v/v) and a spray volume of 187L/ha. Shoot biomass was removed 4 weeks after initial treatment (WAIT) and plants were then allowed to regrow for 4 weeks. After this time period, visual assessments (0 = no control, 100 = complete control) on shoot regrowth were performed and shoot regrowth and root biomass were collected. Samples were placed in a forced air oven at 70 C for 3 days and dry weights recorded. Diflufenzopyr Timing Study This study was a 4 (diflufenzopyr timings) by 2 (glyphosate or imazapyr) by 4 (rates) factorial in a completely randomized design. Diflufenzopyr was selected specifically for this study because it has been determined through research by English (1998) and Gaffney (1996) to have caused a greater level of cogongrass bud break. Treatments for this study included diflufenzopyr applied at a rate of 0.22 kg-ai/ha 3 days prior, in conjunction, or 3 days after the application of glyphosate or imazapyr. Glyphosate and imazapyr rates included 0.0, 0.43, 0.84, or 1.68 kg-ai/ha, and 0.0, 0.14, 0.28, or 0.56 kg-ai/ha, respectively. Three diflufenzopyr timings were chosen because it was uncertain when axillary shoot growth would be stimulated. Controls consisted of untreated plants, only surfactant treatment, and diflufenzopyr alone treatments. Experiment one occurred from 24 October 2005 19 December 2005 and experiment two occurred from 12 May 2006 7 July 2006. TP1PT Metro mix Agricultural Lite Mix TP2PT ScottsPP Osmocote 14-14-14 30

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Growth Regulator Study This study was a 4 (growth regulating herbicides) by 2 (glyphosate or imazapyr) by 4 (rates) factorial in a completely randomized design. In this study, PGR herbicides were applied to actively growing cogongrass in conjunction with glyphosate and imazapyr. The rates for dicamba, 2,4-D, triclopyr, and quinclorac were 0.56, 1.12, 0.56, and 1.4 kg-ai/ha, respectively. The glyphosate and imazapyr rates were the same as reported for the diflufenzopyr study. Experiment one occurred from 7 March 2006 to 2 May 2006 and experiment two occurred from 28 April 2006 to 23 June 2006. Statistical Analysis The data were analyzed using proc GLM program in SAS 9.1. Models for the independent variables (experiment, growth regulating herbicides or timing, herbicide, and rate) were determined using the dependent variables (visual evaluations, and shoot regrowth and rhizome/root biomass harvests). Data are reported as p-values for interaction and means with 95% confidence intervals for statistical difference. All studies were conducted twice with 4 replications. Results Diflufenzopyr Timing Study Analysis of variance indicated a significant (p < 0.05) treatment by experiment interaction therefore experiments are presented separately. Experiment one Visual evaluation. There was a significant (p < 0.05) three-way interaction among diflufenzopyr timing, herbicide, and herbicide rate for the visual evaluation (Table 2-1). When glyphosate was applied alone at 0.43 kg-ai/ha, or when diflufenzopyr was applied 3 days prior to, or 3 days after glyphosate at this rate, < 8% control was observed (Table 2-2). However, when 31

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glyphosate was applied tank-mixed with diflufenzopyr, nearly 50% control was observed. This tank-mixed treatment did not differ from the previously mentioned diflufenzopyr application occurring 3 days after glyphosate application. Glyphosate (0.84 kg-ai/ha) applied alone or with diflufenzopyr applied 3 days after provided no observed control. Treatments tank-mixed at this rate (0.84 kg-ai/ha) provided more control compared to glyphosate alone. Diflufenzopyr had no effect on glyphosate at the highest rate (1.68 kg-ai/ha). Imazapyr (0.14 kg-ai/ha) with diflufenzopyr applied 3 days before or tank-mixed provided more cogongrass control compared to imazapyr alone (Table 2-2). Diflufenzopyr had no effect on the 2 highest imazapyr rates (0.28 and 0.56 kg-ai/ha). The diflufenzopyr treatments did not differ across rates, all providing > 88% control with any application timing. Shoot regrowth. There were significant two-way interactions (p < 0.05) between all treatment variables (timing and herbicide, herbicide and rate, and timing and rate) for shoot regrowth in experiment 1 (Table 2-1). No glyphosate treatments reduced shoot regrowth compared to the untreated controls (0.8 0.4 grams/pot) (Table 2-3). Diflufenzopyr, when tank-mixed with glyphosate (0.43 kg-ai/ha), reduced regrowth compared to glyphosate alone. However, diflufenzopyr had no effect at the highest rates (0.84 and 1.68 kg-ai/ha). Herbicide rate had no effect for most glyphosate treatments, glyphosate (1.68 kg-ai/ha) alone or with diflufenzopyr applied 3 days after are the exceptions. These treatments reduced shoot regrowth compared to these same treatments at lower rates. All imazapyr treatments reduced shoot regrowth compared to the untreated control (0.8 0.4 grams/pot) (Table 2-3). The addition of diflufenzopyr to the lower imazapyr rate (0.14 kg-ai/ha) greatly reduced shoot regrowth to < 0.1 grams/pot. Diflufenzopyr had no effect when the 32

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rate of imazapyr increased (0.28 and 0.56 kg-ai/ha). However regrowth for all treatments at these rates did not exceed 0.1 grams/pot. Rhizome biomass. There was a high level of variability within experiment 1, resulting in no differences among treatments (Table 2-1). Treatments also did not differ in comparison to the untreated controls (8.8 10.0 grams/pot) (Table 2-4). Experiment two Overall model variance for experiment 2 parameters, including visual evaluation, shoot regrowth biomass and rhizome/root biomass are listed in Table 2-5. Visual evaluation. There was a significant (p < 0.05) three-way interaction among timing, herbicide, and herbicide rate for the visual evaluation (Table 2-5). At any rate or diflufenzopyr timing, < 50% control was observed for glyphosate (Table 2-6). The addition of diflufenzopyr had no effect at the lowest and highest glyphosate rates (0.43 and 1.68 kg-ai/ha). When glyphosate (0.84 g-ai/ha) was applied alone there was almost no control. Diflufenzopyr applied 3 days before or 3 days after glyphosate provided more control compared to glyphosate alone. Glyphosate alone at the lowest and highest rates (0.43 and 1.68 kg-ai/ha) provided more control compared to the intermediate rate of glyphosate (0.84 kg-ai/ha). Cogongrass control from imazapyr in experiment 2 was influenced greatly by diflufenzopyr timing treatments (Table 2-7). Greater than 90% control was observed with imazapyr (0.14 kg-ai/ha) when tank-mixed with diflufenzopyr. Similar levels of control were also observed with the 2 highest imazapyr rates (0.28 and 0.56 kg-ai/ha) when tank-mixed with diflufenzopyr. Control observed with imazapyr alone at 0.28 kg-ai/ha did not differ from the tank-mixed treatments, but it also did not differ from treatments with diflufenzopyr applied 3 days before or 3 days after. The effect of diflufenzopyr was not observed at the highest rate (0.56 kg-ai/ha). However, all treatments at this rate provided > 50% control. Control from the lowest 33

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and highest rates of imazapyr (0.14 and 0.56 kg-ai/ha), with diflufenzopyr applied 3 days after, exceeded the control provided by the intermediate rate (0.28 kg-ai/ha) with the same treatment. Shoot regrowth. There was significant (p < 0.05) three-way interaction among timing, herbicide, and herbicide rate for the visual evaluation (Table 2-5). Only 2 glyphosate treatments reduced shoot regrowth compared to the untreated controls (0.8 0.2 grams/pot); diflufenzopyr applied 3 days after glyphosate (0.43 kg-ai/ha) and glyphosate alone (0.84 kg-ai/ha) (Table 2-7). In each of these treatments the shoot regrowth more than doubled the biomass of the untreated control. Glyphosate applied alone (0.43 and 0.84 kg-ai/ha) either yielded the most regrowth, or did not differ from the treatment with the most regrowth within the rate; the other treatments included diflufenzopyr applied 3 days after glyphosate (0.43 kg-ai/ha) or tank-mixed at 0.84 kg-ai/ha. Diflufenzopyr had no effect on glyphosate at the highest rate (1.68 kg-ai/ha). Four imazapyr treatments reduced cogongrass regrowth compared to the untreated control (0.8 0.2 grams/pot); diflufenzopyr applied tank-mixed with any rate, or 3 days before imazapyr (0.56 kg-ai/ha) (Table 2-7). Shoot regrowth was negligible when diflufenzopyr was tank mixed with imazapyr (0.14 and 0.28 kg-ai/ha). While diflufenzopyr tank-mixed with imazapyr (0.28 kg-ai/ha) yielded less regrowth compared to diflufenzopyr applied 3 days before or 3 days after, imazapyr alone did not differ from any diflufenzopyr treatments. No effect was observed with diflufenzopyr at the highest rate (0.56 kg-ai/ha) Rhizome biomass. There was a significant (p < 0.05) two-way interaction between herbicide and herbicide rate (Table 2-5). Timing was not significant when examined alone for the rhizome biomass. No treatments reduced rhizome biomass compared to the untreated control (8.2 6.4) (Table 2-8). Diflufenzopyr reduced rhizome biomass when applied with glyphosate (0.84 kg-ai/ha) compared to glyphosate alone (Table 2-8). Applied tank-mixed or 3 days after 34

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glyphosate (0.84 kg-ai/ha), diflufenzopyr reduced rhizome biomass compared to the same treatment at the higher glyphosate rate (1.68 kg-ai/ha). Diflufenzopyr had no effect on rhizome biomass when mixed with imazapyr. Growth Regulator Study Analysis of variance indicated a significant (p < 0.05) treatment by experiment interaction for the shoot regrowth, therefore experiments are presented separately. Experiment one Overall model variance for experiment 2 parameters, including visual evaluation, shoot regrowth biomass, and rhizome/root biomass are listed in Table 2-9. Visual evaluation. There was a significant (p < 0.05) three-way interaction with growth regulator, herbicide, and herbicide rate for the visual evaluation (Table 2-9). When applied in the absence of glyphosate or imazapyr, < 20% control was observed for the PGR herbicides (Table 2-10). Although glyphosate control never exceeded 25% for the two lowest rates (0.43 and 0.84 kg-ai/ha), the addition of PGR herbicides had no effect on glyphosate. Glyphosate alone at 1.68 kg-ai/ha provided nearly 90% control. The addition of PGR herbicides to this rate of glyphosate decreased control by greater than 50%. Cogongrass control with imazapyr varied greatly (Table 2-10). Imazapyr applied alone, regardless of rate, had < 30% control. Dicamba with imazapyr at the lowest rate (0.14 kg-ai/ha) provided almost no observed control. Imazapyr (0.28 kg-ai/ha) with any PGR herbicide provided nearly 70-90% control compared to imazapyr in the absence of PGR herbicides, although dicamba did not differ from imazapyr alone. An even higher level of control was also observed at any rate of imazapyr with 2,4-D. With the exception of 2,4-D, imazapyr treatments at the highest rate (0.56 kg-ai/ha) did not exceed 65% control. 35

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Shoot regrowth. There was a significant (p < 0.05) interaction among growth regulator, herbicide, and herbicide rate for the shoot regrowth in experiment 2 (Table 2-9). While PGR herbicides alone did not differ from the untreated control, triclopyr had less regrowth compared to quinclorac. The addition of most PGR herbicides to glyphosate at the lowest rate (0.43 kg-ai/ha) had no effect, with the exception of triclopyr. This triclopyr treatment tripled the amount of shoot biomass compared to triclopyr alone and double the biomass compared to glyphosate alone. Plant growth regulating herbicides also had no effect when glyphosate rate increased to 0.84 kg-ai/ha. Glyphosate alone at 1.68 kg-ai/ha reduced shoot regrowth to < 0.1 grams/pot. The PGR herbicide treatments failed to provide this much reduction. Overall, cogongrass regrowth with imazapyr was reduced compared to glyphosate treatments (Table 2-12). Imazapyr alone did not differ from the untreated controls. Most imazapyr treatments in conjunction with PGR herbicides provided < 0.4 grams of regrowth per pot. Plant growth regulating herbicides with imazapyr at 0.28 kg-ai/ha reduced shoot regrowth compared to imazapyr alone. Minimal shoot regrowth occurred with 2,4-D and imazapyr at the lowest rate (0.14 kg-ai/ha), and almost no regrowth occurred at the higher rates (0.28 and 0.56 kg-ai/ha). Imazapyr and quinclorac had more shoot regrowth at the highest rate (0.56 kg-ai/ha) compared to the 2 lower rates (0.14 and 0.28 kg-ai/ha). Rhizome biomass. There was a high level of variability within experiment 1, resulting in only significant (p < 0.05) distinction within PGR herbicides (Table 2-10). Majority of the glyphosate or imazapyr treatments did not differ in rhizome biomass compared to the untreated controls (Table 2-12). Triclopyr alone and glyphosate alone (1.68 kg-ai/ha) reduced rhizome biomass. Imazapyr alone (0.28 and 0.56 kg-ai/ha), or imazapyr (0.28 kg-ai/ha) with 2,4-D or quinclorac also reduced rhizome biomass compared to the untreated control. Rate of glyphosate 36

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or imazapyr and most PGR herbicides had no effect on rhizome biomass compared to glyphosate or imazapyr alone. Experiment two Overall model variance for experiment 2 parameters, including visual evaluation, shoot regrowth biomass and rhizome/root biomass are listed in Table 2-13. Visual evaluation. There was a significant (p < 0.05) three-way interaction with growth regulator, herbicide, and herbicide rate for the visual evaluation (Table 2-13). When triclopyr was applied in the absence of glyphosate or imazapyr almost no control was observed (Table 2-14). Dicamba and quinclorac alone provide more control compared to untreated plants. The remaining PGR herbicides alone did not differ from the untreated controls. No glyphosate treatments exceeded 55% control. The effect of PGR herbicides was not observed at any rate of glyphosate. Also, there was no difference between the level of control provided by the PGR herbicides alone or in conjunction with glyphosate. Similar, levels of control were observed with most imazapyr treatments, and many treatments did not exceed 35% control (Table 2-14). However, imazapyr at the two highest rates (0.28 and 0.56kg-ai/ha) with 2,4-D provided more control, almost 50% at 0.28 kg-ai/ha and almost 90% at the highest imazapyr rate. Similar to glyphosate results, the level of control provided by the PGR herbicides alone did not differ from the imazapyr/PGR herbicide treatments, the exception being 2,4-D with the highest rate of imazapyr. Shoot regrowth. There was a high level of variability within experiment 2 resulting in no differences among treatments (Table 2-14). Only triclopyr with glyphosate at the lowest rate (0.43 kg-ai/ha) yielded less shoot biomass compared to the untreated controls (Table 2-15). 37

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Rhizome biomass. There was no significant (p < 0.05) interaction among growth regulator, herbicide, and herbicide rate (Table 2-11). Also, no treatments reduced rhizome mass compared to the untreated controls (Table 2-16). Discussion Acceptable cogongrass control is defined as having > 80% reduction in rhizome biomass 2 years after treatment (Willard et al. 1996). This level of control can best be achieved if the management method targets the rhizomes and all viable tillers (Tanner et al. 1992, Willard et al. 1997). In these studies, growth regulating herbicides in conjunction with either glyphosate or imazapyr targeted cogongrass rhizomes, to affect control. However, lack of consistent distinction in rhizome dry weight for the diflufenzopyr timing experiments and the growth regulator experiments leads to a closer examination of the visual evaluation and the shoot regrowth dry weight. Thus, acceptable control, in this study, is defined as > 80% injury or visual reduction, 8 weeks after initial treatment. Despite some of the discrepancies with both experiments in the diflufenzopyr timing study, there are some consistent trends with the data. The best control in the diflufenzopyr study came from imazapyr treatments (0.56 kg-ai/ha), which provided greater than 75% control with diflufenzopyr. However, it was questionable whether diflufenzopyr made any difference with these treatments in experiment 1. Extended control with imazapyr is common with cogongrass management as a result of residual activity of the herbicide (Johnson et al. 1997, Willard et al. 1997). In experiment 1, imazapyr had acceptable control regardless of whether diflufenzopyr was applied. However, in experiment 2, acceptable control was only achieved with imazapyr if diflufenzopyr was included (> 90% control). Regardless of the experiment, imazapyr treatments that were tank-mixed with diflufenzopyr yielded 0.1 grams of regrowth or less. 38

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Glyphosate treatments provided unacceptable levels of regrowth control in both experiments. Some glyphosate treatments at 0.43 and 0.84 kg-ai/ha actually increased shoot regrowth when applied alone, compared to some diflufenzopyr applications. Increased growth is a symptom that, although rare, sometimes follows a glyphosate application (Marrs et al. 1989). As there is no prior documentation of discrepancies using diflufenzopyr, the inconsistencies in the diflufenzopyr experiments could have occurred as a result of experimental timing. Experiment 1 occurred in the fall, whereas experiment 2 occurred in the spring. While both of the experiments occurred in a temperature controlled greenhouse, inconsistent artificial light, caused by a faulty light system, may have been the problem. It is possible that experimental differences occurred as a result of day-length, even if only for a short period. Day-length is just one of the factors responsible for translocation of photosynthates in the leaves down to the rhizomes in preparation for winter dormancy (Gaffney 1996). Herbicide applications in the fall tend to result in greater efficacy compared to spring treatments (> 20% more control, 12 months after treatment) for both glyphosate and imazapyr as they are actively translocated with the photosynthates to the rhizomes (Tanner et al. 1992, Gaffney 1996, Johnson et al. 1997). The growth regulator study indicated imazapyr (0.56 kg-ai/ha) and 2,4-D provided approximately 90% control or greater. This treatment decreased shoot regrowth when compared to untreated plants. Collectively, these experiments suggest the addition/combination of dicamba, quinclorac, or triclopyr with glyphosate or imazapyr for cogongrass control does not provide any advantage. The advantage of adding/combining PGR herbicides to glyphosate or imazapyr was only observed with imazapyr in conjunction with 2,4-D or diflufenzopyr. However, the overall inconsistencies may be due to an insufficient interval to increase shoot:rhizome ratio, a problem 39

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that is addressed in the field study. Other explanations include a decrease in translocation or general inconsistencies with the PGR herbicides. Table 2-1. Overall model variance for the visual evaluation, shoot regrowth biomass, and rhizome biomass 8 weeks after initial treatment in the cogongrass diflufenzopyr timing Experiment 1. Variables Visual evaluation p-value Shoot regrowth p-value Rhizome p-value ExperimentP1P < 0.0001 < 0.0001 < 0.0001 Timing < 0.0001 < 0.0001 0.0880 Herbicide < 0.0001 < 0.0001 0.8797 Timing*herbicide 0.4016 0.0004 0.2406 Herbicide rate < 0.0001 < 0.0001 0.0886 Timing*herbicide rate 0.0026 0.0350 0.0865 Herbicide*herbicide rate < 0.0001 < 0.0001 0.2860 Timing*herbicide*herbicide rate 0.0070 0.0585 0.3139 Rep 0.9653 0.7309 0.4316 P1PExperiment comparison between experiment 1 and experiment 2 for the cogongrass diflufenzopyr study. Table 2-2. Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 1. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56 % Control Absent 0 0P1P 0 0 60 18 80 8 93 6 98 6 3 days prior 5 10 20 22 55 26 95 6 98 6 100 0 Tank-mix 48 32 38 30 35 26 95 6 98 6 100 0 3 days after 8 10 0 0 68 22 88 10 95 6 95 6 P1PMeans followed by 95% confidence interval. Table 2-3. Cogongrass shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 1. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56 Grams/pot Absent 1.7 0.8P1P 1.6 0.4 0.4 0.4 0.1 0 < 0.1 0 < 0.1 0 3 days prior 1.0 0.6 0.7 0.4 0.4 0.4 < 0.1 0 < 0.1 0 < 0.1 0 Tank-mix 0.3 0.2 0.6 0.6 0.3 0.2 < 0.1 0 < 0.1 0 < 0.1 0 3 days after 1.2 0.6 1.2 0.2 0.2 0.2 < 0.1 0 < 0.1 0 < 0.1 0 P1PMeans followed by 95% confidence interval. 40

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Table 2-4. Cogongrass rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 1. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56 Grams/pot Absent 9.6 1.4P1P 11.6 2.8 5.7 3.4 9.5 1.6 6.5 4.4 4.5 2.8 3 days prior 7.7 0.6 4.1 1.2 6.2 3.4 6.9 2.8 7.3 1.4 3.9 0.8 Tank-mix 3.6 2.0 6.0 3.6 7.0 1.2 7.4 2.4 6.1 4.8 7.5 3.6 3 days after 7.8 2.6 7.2 2.2 7.2 2.0 10.1 3.4 6.0 1.6 6.9 3.8 P1PMeans followed by 95% confidence interval. Table 2-5. Overall model variance for the visual evaluation, shoot regrowth biomass, and rhizome biomass 8 weeks after initial treatment in the cogongrass diflufenzopyr timing Experiment 2. Variables Visual evaluation p-value Shoot regrowth p-value Rhizome p-value ExperimentP1P < 0.0001 < 0.0001 < 0.0001 Timing 0.0013 0.2927 0.7981 Herbicide < 0.0001 < 0.0001 < 0.0001 Timing*herbicide < 0.0001 0.0335 0.2406 Herbicide rate 0.1004 0.9424 0.1719 Timing*herbicide rate 0.3764 0.1210 0.1562 Herbicide*herbicide rate 0.0117 0.0165 0.0446 Timing*herbicide*herbicide rate 0.0478 0.0016 0.0540 Rep 0.7654 0.7215 0.8715 P1PExperiment comparison between experiment 1 and experiment 2 for the cogongrass diflufenzopyr study. Table 2-6. Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 2. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56 % Control Absent 40 14P1P 10 8 28 6 35 30 53 44 50 40 3 days prior 45 12 40 16 38 28 45 10 38 18 90 12 Tank-mix 33 6 30 24 13 16 90 8 95 10 98 6 3 days after 23 18 35 10 30 24 60 14 30 14 75 30 P1PMeans followed by 95% confidence interval. 41

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Table 2-7. Cogongrass shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings for Experiment 2. Glyphosate (kg-ai/ha)P P Imazapyr (kg-ai/ha) Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56 Grams/pot Absent 1.0 1.0P1P 2.0 0.4 1.4 0.8 1.0 0.4 0.4 0.4 0.8 0.8 3 days prior 1.0 0.4 1.1 0.4 1.3 0.8 1.0 0.4 1.0 0.6 0.1 0.2 Tank-mix 1.0 0.2 1.1 0.6 2.2 1.0 0.1 0.2 < 0.1 0 < 0.1 0 3 days after 2.1 0.4 0.7 0.4 1.7 1.4 0.5 0.4 0.9 0.4 0.4 0.6 P1PMeans followed by 95% confidence interval. Table 2-8. Cogongrass rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings for Experiment 2. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56 Grams/pot Absent 3.2 2.2P1P 10.6 5.6 7.7 7.2 3.6 1.6 2.1 1.4 3.6 1.0 3 days prior 3.9 2.0 3.6 1.6 7.1 5.4 4.2 2.4 5.6 4.8 5.6 4.8 Tank-mix 4.9 2.6 3.7 1.2 11.2 5.8 3.7 2.6 1.5 0.8 2.6 1.4 3 days after 9.1 4.4 2.4 1.0 9.0 2.4 2.5 1.8 2.3 0.8 2.8 1.4 P1PMeans followed by 95% confidence interval. Table 2-9. Overall model variance for the visual evaluation, shoot regrowth biomass, and rhizome biomass 8 weeks after initial treatment in the cogongrass growth regulator Experiment 1. Variables Visual evaluation p-value Shoot regrowth p-value Rhizome p-value ExperimentP1P 0.0812 0.0014 0.9471 Growth regulator < 0.0001 0.0179 0.0799 Herbicide < 0.0001 < 0.0001 0.6256 Growth regulator*herbicide < 0.0001 0.0101 0.3549 Rate < 0.0001 0.0657 0.2569 Growth regulator* herbicide rate < 0.0001 < 0.0001 0.4292 Herbicide*herbicide rate < 0.0001 0.0018 0.4679 Growth regulator*herbicide*herbicide rate 0.0045 0.0247 0.1147 Rep 0.2629 0.3550 0.9058 P1PExperiment comparison between experiment 1 and experiment 2 for the cogongrass growth regulator study. 42

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Table 2-10. Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by plant growth regulating herbicides in Experiment 1. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Growth regulator ControlP1P 0.43 0.84 1.68 0.14 0.28 0.56 % Control Absent 0 0P2P 23 12 5 6 88 10 25 20 20 20 28 26 2,4-D 15 6 13 10 18 28 23 26 78 10 90 8 100 0 Dicamba 10 0 10 8 8 10 25 20 5 8 68 30 40 32 Quinclorac 0 0 20 20 13 10 28 48 38 10 75 32 20 8 Triclopyr 15 10 5 6 10 14 25 20 30 22 90 12 63 20 P1PGrowth regulating herbicides applied alone in absence of glyphosate or imazapyr.P 2PMeans followed by 95% confidence interval. Table 2-11. Cogongrass shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by plant growth regulating herbicides in Experiment 1. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Growth regulator ControlP1P 0.43 0.84 1.68 0.14 0.28 0.56 Grams/pot Absent 1.0 0.4P2P 0.8 0.0 1.0 0.6 <0.1 0 0.7 0.2 0.7 0.2 0.5 0.4 2,4-D 0.7 1.2 0.7 0.2 1.3 0.2 0.5 0.2 0.2 0.0 <0.1 0 <0.1 0 Dicamba 0.8 0.2 0.7 0.2 1.5 0.8 0.6 0.4 1.1 0.4 0.2 0.2 0.3 0.2 Quinclorac 1.2 0.4 0.9 0.6 0.8 0.4 1.6 1.4 0.4 0.2 0.2 0.2 0.9 0.2 Triclopyr 0.5 0.2 1.6 0.6 1.0 0.8 0.7 0.6 0.4 0.2 0.1 0.0 0.2 0.2 P1PGrowth regulating herbicide applied alone in absence of glyphosate or imazapyr. P2PMeans followed by 95% confidence interval. Table 2-12. Cogongrass rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by plant growth regulating herbicides in Experiment 1. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Growth regulator ControlP1P 0.43 0.84 1.68 0.14 0.28 0.56 Grams/pot Absent 6.1 2.2P2P 4.0 2.6 4.0 0.6 0.9 0.6 4.0 1.8 2.2 0.2 2.9 0.2 2,4-D 4.3 3.8 3.6 1.2 4.3 3.6 4.6 3.6 3.5 2.8 3.7 1.0 3.1 1.8 Dicamba 3.4 1.8 5.7 4.4 4.8 3.6 4.5 1.2 7.6 3.0 4.7 3.4 3.2 2.0 Quinclorac 6.9 2.4 5.1 2.8 4.3 14.6 7.3 4.0 5.9 3.6 2.8 1.4 5.5 2.2 Triclopyr 3.0 0.6 7.9 6.8 5.5 3.4 3.5 2.2 3.1 2.6 3.3 3.2 7.9 5.2 P1PGrowth regulating herbicide applied alone in absence of glyphosate or imazapyr. P2PMeans followed by 95% confidence interval. 43

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Table 2-13. Overall model variance for the visual evaluation, shoot regrowth biomass, and rhizome biomass 8 weeks after initial treatment in the cogongrass growth regulator Experiment 2. Variables Visual evaluation p-value Shoot regrowth p-value Rhizome p-value ExperimentP1P 0.0812 0.0014 0.9471 Growth regulator < 0.0001 0.1589 0.3652 Herbicide 0.0449 0.8143 0.4313 Growth regulator*herbicide 0.0026 0.0596 0.0538 Rate 0.0025 0.1310 0.0536 Growth regulator* herbicide rate 0.0749 0.9698 0.8537 Herbicide*herbicide rate 0.0748 0.1386 0.9968 Growth regulator*herbicide*herbicide rate 0.0235 0.4928 0.4309 Rep 0.9945 0.8581 0.9764 P1PExperiment comparison between experiment 1 and experiment 2 for the cogongrass growth regulator study. Table 2-14. Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influences by plant growth regulating herbicides in Experiment 2. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Growth regulator ControlP1P 0.43 0.84 1.68 0.14 0.28 0.56 % Control Absent 0 0P2P 30 18 18 10 15 6 23 18 20 35 12 2,4-D 38 6 33 6 25 18 30 14 25 20 48 6 88 18 Dicamba 25 20 20 14 28 18 35 10 28 10 20 14 30 22 Quinclorac 30 8 43 10 35 24 53 34 35 12 18 12 25 10 Triclopyr 10 12 25 10 20 12 25 18 15 6 20 18 35 32 P1PGrowth regulating herbicides applied alone or in the absence of glyphosate or imazapyr. P2PMeans followed by 95% confidence interval. Table 2-15. Cogongrass shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influences by plant growth regulating herbicides in Experiment 2. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Growth regulator ControlP1P 0.43 0.84 1.68 0.14 0.28 0.56 Grams/pot Absent 1.4 0.4P2P 0.8 0.8 1.1 0.0 1.1 0.4 1.1 0.8 1.7 2.4 0.7 0.4 2,4-D 0.5 0.2 0.9 0.4 1.3 1.0 1.2 0.8 1.1 0.6 0.5 0.0 0.2 0.2 Dicamba 0.7 0.4 1.0 0.4 0.9 0.6 0.6 0.2 1.0 0.6 1.2 0.6 0.8 0.4 Quinclorac 0.7 0.2 0.6 0.2 0.4 0.2 0.5 0.4 0.7 0.4 1.5 0.8 0.7 0.4 Triclopyr 1.8 0.8 0.7 0.2 1.0 0.4 1.0 0.6 1.3 0.8 1.0 0.6 0.6 0.4 P1PGrowth regulating herbicides applied alone or in the absence of glyphosate or imazapyr. P2PMeans followed by 95% confidence interval. 44

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Table 2-16. Cogongrass rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influences by plant growth regulating herbicides in Experiment 2. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Growth regulator ControlP1P 0.43 0.84 1.68 0.14 0.28 0.56 Grams/pot Absent 5.9 2.2P2P 5.3 4.6 6.6 1.6 5.0 1.0 4.6 2.6 4.5 3.4 2.7 0.6 2,4-D 2.9 1.2 4.8 0.8 6.8 4.8 5.5 2.4 4.1 2.0 3.2 1.2 3.5 0.6 Dicamba 3.9 2.4 7.6 6.4 6.5 3.6 3.5 1.4 5.3 1.8 4.3 1.6 3.3 2.2 Quinclorac 3.5 2.2 3.7 1.0 2.5 1.8 2.0 1.2 3.8 1.4 7.7 3.4 3.0 1.8 Triclopyr 6.3 2.6 4.7 1.2 4.7 1.6 3.1 1.2 5.3 2.8 4.2 1.6 2.8 1.0 P1PGrowth regulating herbicides applied alone or in the absence of glyphosate or imazapyr. P2PMeans followed by 95% confidence interval. 45

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CHAPTER 3 THE INFLUENCE OF GROWTH REGULATOR HERBICIDES ON THE EFFICACY OF GLYPHOSATE AND IMAZAPYR ON TORPEDOGRASS UNDER GREENHOUSE CONDITIONS Introduction Torpedograss is an old world Eurasian plant and is most frequently found near or in aquatic sites (Holm et al. 1977). Since 1992, Florida Department of Environmental Protection has ranked torpedograss as the 2PndP most abundant plant in Florida lakes (Schardt 1992, Schardt personal communication, February 2007). Torpedograss can also be found on terrestrial areas such as golf courses and roadsides (McCarty et al. 1993). The presence of torpedograss is problematic in Florida because it interrupts flood control, irrigation and turf production (Shilling and Haller 1989, McCarty et al. 1993). The rapid growth and extensive rhizome system are the primary issues with torpedograss invasiveness. The rhizome system comprises 70 to 90% of total biomass (Smith et al. 1999). When fragmented, 92 to 96% of rhizome buds can regenerate when temperatures range from 20 to 35C (Hossain et al. 2001). New buds are continuously produced along the entire length of the rhizomes indicating very weak apical dominance (Wilcut et al. 1988a). Since all of the nodes found on the rhizome system can be viable, complete control of torpedograss requires total removal of all viable tillers and rhizomes (Sutton 1996, Smith et al. 1999). Most torpedograss management studies come with mixed success, with few showing 100% long term control (> 12 months) within time constraints and budgets for the average landowner (Manipura and Somaratne 1974, Willard et al. 1998, Smith et al. 1999). Studies have most commonly used glyphosate and imazapyr for torpedograss control (Baird et al. 1983, Shilling and Haller 1989, Willard et al. 1998, Smith et al. 1999, Hanlon and Langeland 2000). 46

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Long term control (>12 months) has never been reported for torpedograss using glyphosate [N-(phosphonomethyl)glycine] with a single application (Manipura and Somaratne 1974, Shilling and Haller 1989, Smith et al. 1999). Limited control from glyphosate is often attributed to the aquatic habitat of torpedograss as the herbicide only reaches the emergent portion of the plant. Although the emergent portion of the plant was controlled, regrowth from rhizomes and submerged stems segments occurred within a few months (Baird et al. 1983). Smith et al. (1999) concluded that high water levels inhibit foliar interception of glyphosate and control correlated with foliar exposure to water level ratio. To achieve 90% control (5 weeks after initial treatment), a glyphosate application rate of 2.24 kg-ai/ha was needed to be intercepted by at least 40% of the foliage. Lower rates correlated with a higher percentage of foliage cover to achieve similar results (Smith et al. 1999). Imazapyr applications on torpedograss have shown similar issues with submergence and in turn, less control (Hanlon and Langeland 2000). Inconsistencies in data presented by Hanlon and Langeland (2000) lead the authors to speculate that fluctuating water depth at different experimental sites could have influenced results. While all experiments began in approximately 0.8 meters of water, by the end of the experiment, one study site was considered dry while the remaining sites were flooded. Greater than 95% control was observed at the dry site and < 25% control for the flooded sites. The authors also speculated that thatch levels may have contributed to inconsistent control as the amount of torpedograss tissue exposed to the herbicide may be reduced. This reduction may have been a result of thatch preventing the herbicide from achieving adequate uptake (Hanlon and Langeland 2000). Collectively, results from previous studies indicate poor control of torpedograss with a low percentage of exposed foliar tissue. Therefore, methods to increase control are highly warranted. 47

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If torpedograss rhizomes could be chemically stimulated to increase shoot production, allowing more of the plant to be exposed, then herbicide applications of glyphosate or imazapyr could potentially be more effective. Increased shoot production has been accomplished using growth regulating herbicides, such as dicamba on wheat, Triticum aestivum (Bahieldin et al. 2000). These herbicides interfere with growth hormone functions and have similar modes of action and selectivity (Anderson 1996). Although the true mode of action for some of these herbicides is unknown, it is speculated that some mimic auxins in an unregulated fashion in plants, while others block the transport of auxins (Anderson 1996, WSSA 2002, Lym and Deibert 2005). Several herbicides interfere with normal auxin function in plants. These include not only dicamba, but also triclopyr, 2,4-D, quinclorac, and diflufenzopyr, as well as others (Anderson 1996, WSSA 2002). Previous research by English (1998) studied the impact of these herbicides on bud break in cogongrass and found that diflufenzopyr was most effective on other invasive grasses, such as cogongrass. Application timing of diflufenzopyr appears to be critical for control (Ketchersid and Senseman 1998). The combination of diflufenzopyr and dicamba proved more phytotoxic to other broadleaves such as field bindweed (Convovulus arvense L.) and velvetleaf (Abutilon theophrasti Medic.) when diflufenzopyr was applied 3 days before the herbicide compared to diflufenzopyr in conjunction with or after application (Ketchersid and Senseman 1998). Since torpedograss occurs in aquatics, an area where most control methods are not feasible or may be ineffective; the use of growth regulating herbicides in conjunction with current control methods warrants research. The application timing of diflufenzopyr and the combination of glyphosate or imazapyr with growth regulating herbicides has never been studied on 48

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torpedograss. Thus, this study has two objectives: 1.) determine the effect of diflufenzopyr application timing on the efficacy of glyphosate and imazapyr on torpedograss, and 2.) determine the effect of growth regulating herbicides, other than diflufenzopyr, on the efficacy of glyphosate and imazapyr on torpedograss. Materials and Methods Torpedograss plants were established from rhizomes that were obtained from local Gainesville populations. Plants were grown under greenhouse conditions with the following environmental parameters: 12 hr day, 12 hr night, temperature 30/20C. Torpedograss was grown in 3L pots with commercial potting soilTP3PT and amended with slow-release fertilizerTP4PT. Plants were grown for 8 to 10 weeks to ensure a dense and healthy rhizome mass. Treatments for both studies were applied using a standard small plot sprayer with appropriate nonionic surfactant (0.25% v/v) and a spray volume of 187L/ha. Shoot biomass was removed 4 weeks after initial treatment (WAIT) and plants were then allowed to regrow for 4 weeks. After this time period, visual assessments (0 = no control, 100 = complete control) on shoot regrowth were performed and shoot regrowth and root biomass were collected. Samples were placed in a forced air oven at 70 C for 3 days and dry weights recorded. Diflufenzopyr Timing Study This study was a 4 (diflufenzopyr timings) by 2 (glyphosate or imazapyr) by 4 (rates) factorial in a completely randomized design. Diflufenzopyr was selected specifically for this study because it has been determined through research by English (1998) and Gaffney (1996) to have caused a greater level bud break in other invasive grasses, such as cogongrass. Treatments for this study included diflufenzopyr applied at a rate of 0.22 kg-ai/ha 3 days prior, in TP3PT Metro mix Agricultural Lite Mix TP4PT ScottsPP Osmocote 14-14-14 49

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conjunction with, or 3 days after the application of glyphosate or imazapyr. Glyphosate and imazapyr rates included 0.0, 0.43, 0.84, or 1.68 kg-ai/ha and 0.0, 0.14, 0.28, or 0.56 kg-ai/ha, respectively. Three diflufenzopyr timings were chosen because it is uncertain when axillary shoot growth will be stimulated with diflufenzopyr. Controls consisted of untreated plants, only surfactant treatment, and diflufenzopyr alone treatments. Experiment one occurred from 2 February 2006 to 10 April 2006 and experiment two occurred from 20 March 2006 to 15 May 2006. Growth Regulator Study This study was a 4 (growth regulating herbicides) by 2 (glyphosate or imazapyr) by 4 (rates) factorial in a completely randomized design. In this study, PGR herbicides were applied to actively growing cogongrass in conjunction with glyphosate and imazapyr. The rates for dicamba, 2,4-D, triclopyr, and quinclorac were 0.56, 1.12, 0.56, and 1.4 kg-ai/ha, respectively. The glyphosate and imazapyr rates were the same as reported for study one. Experiment one occurred from 7 March 2006 2 May 2006 and experiment two occurred from 10 May 2006 5 July 2006. Statistical Analysis Data were analyzed using proc GLM program in SAS 9.1. Models for the independent variables (experiment, growth regulating herbicides or timing, herbicide, and rate) were determined using the dependent variables (visual evaluations, and shoot regrowth and rhizome/root biomass harvests). Data are reported as p-values for interaction and means with 95% confidence intervals for statistical difference. All studies were conducted twice with 4 replications. 50

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Results Diflufenzopyr Timing Study Analysis of variance indicated a significant treatment by experiment interaction therefore experiments are presented separately. Experiment one Visual evaluation. There was significant (p < 0.05) three-way interaction with timing, herbicide, and herbicide rate for the visual evaluation (Table 3-1). Glyphosate treatments did not exceed 50% control (Table 3-2). No effect was observed by adding diflufenzopyr to glyphosate at the lowest and highest rates (0.43 and 1.68 kg-ai/ha). Diflufenzopyr applied to glyphosate at 0.84 kg-ai/ha either decreased the level of control provided by glyphosate alone or did not differ from it. A rate effect was observed when diflufenzopyr was applied 3 days before glyphosate. The lowest rate (0.43 kg-ai/ha) had more control compared to the 2 highest rates (0.84 and 1.68 kg-ai/ha). Torpedograss control also never exceeded 50% with imazapyr treatments (Table 3-2). The addition of diflufenzopyr to imazapyr at 0.14 and 0.56 kg-ai/ha had no effect. Diflufenzopyr when tank-mixed with imazapyr at 0.28 kg-ai/ha exceeded the level control observed when it was applied 3 days after. However, no treatments differed from imazapyr alone. Shoot regrowth. There was significant (p < 0.05) two-way interaction with herbicide and herbicide rate, but no three-way interaction (Table 3-1). Timing was also a significant (p < 0.05) when examined alone. No treatments reduced shoot regrowth compared to the untreated controls (0.8 0.2 grams/pot) (Table 3-3). Diflufenzopyr had no effect on the shoot regrowth with glyphosate at 0.43 and 0.84 kg-ai/ha, or imazapyr at any rate. When glyphosate (1.69 kg-ai/ha) or imazapyr (0.28 kg-ai/ha) were tank-mixed with diflufenzopyr, 50% less shoot regrowth occurred compared to when diflufenzopyr was applied 3 days after glyphosate or imazapyr. 51

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Rhizome biomass. There was significant (p < 0.05) two-way interaction with herbicide and herbicide rate, but no three-way interaction (Table 3-1). Timing was also a significant (p < 0.05) when examined alone. Rhizome biomass was reduced with only 3 treatments, compared to the untreated control (3.4 1.6 grams/pot). These treatments included glyphosate alone (0.84 kg-ai/ha), imazapyr alone (0.28 kg-ai/ha), and diflufenzopyr applied 3 days before glyphosate (1.68 kg-ai/ha). Diflufenzopyr with glyphosate (0.43 kg-ai/ha) increased the rhizome biomass compared to glyphosate alone. No effect was observed with diflufenzopyr as glyphosate rate increased to 0.84 kg-ai/ha. When diflufenzopyr was applied 3 days after glyphosate at 1.68 kg-ai/ha rhizome biomass more than doubled in comparison to the remaining treatments at this rate. Torpedograss rhizome biomass was not affected by the addition of diflufenzopyr to imazapyr at 0.14 kg-ai/ha. Imazapyr alone reduced rhizome mass in comparison to diflufenzopyr applied 3 days before or 3 days after. Diflufenzopyr tank-mixed with imazapyr at 0.56 kg-ai/ha reduced rhizome mass compared to imazapyr alone. A rate effect was observed with imazapyr alone. The intermediate rate (0.28 kg-ai/ha) had greater rhizome mass compared to the highest and the lowest rates. Experiment two Overall model variance for experiment 2 parameters, including visual evaluation, shoot regrowth biomass, and rhizome/root biomass are listed in Table 3-7. Visual evaluation. There was no twoor three-way interaction for the visual evaluation (Table 3-7). However, herbicide rate was significant (p < 0.05) when examined alone. Diflufenzopyr had no effect in this experiment. Most treatments provided the same level of control at any rate. When diflufenzopyr was applied 3 days before glyphosate, the lowest glyphosate rate (0.14 kg-ai/ha) provided more control compared to the highest rate (1.65 kg-ai/ha) 52

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Shoot regrowth. There was a high level of variability within experiment 2, resulting in no differences among treatments (Table 3-7). Also, no treatments reduced shoot regrowth compared to the untreated control (0.7 0.4) (Table 3-7). Rhizome biomass. There was no twoor three-way interaction for the visual evaluation (Table 3-5). However, herbicide was significant (p < 0.05) when examined alone. Only 3 treatments reduced rhizome mass compared to the untreated control (4.3 0.6 grams/pot); diflufenzopyr applied 3 days before glyphosate (0.14 kg-ai/ha), tank mixed with glyphosate at 0.84 kg-ai/ha, and diflufenzopyr applied 3 days after imazapyr (0.28 kg-ai/ha) (Table 3-8). Diflufenzopyr had no effect on rhizome biomass when combined with glyphosate at the 2 highest rates (0.84 and 1.68 kg-ai/ha) or with imazapyr at the 2 lowest rates (0.14 and 0.28 kg-ai/ha). When diflufenzopyr was applied 3 days before glyphosate (0.14 kg-ai/ha) rhizome biomass was reduced compared to glyphosate alone. A reduction in rhizome biomass was also observed when diflufenzopyr was tank-mixed or applied 3 days after imazapyr at 0.56 kg-ai/ha compared to imazapyr alone. Growth Regulator Study Overall, model variance for experiment 1 parameters, including visual evaluation, shoot regrowth biomass and rhizome/root biomass are listed in Table 3-9. Experiment one Visual evaluation. There was a significant (p < 0.05) three-way interaction with growth regulator, herbicide, and herbicide rate interaction for the visual evaluation (Table 3-9). When PGR herbicides were applied in the absence of glyphosate or imazapyr control did not differ from the untreated plants (Table 3-10). Glyphosate control never exceeded 40%, and the addition of PGR herbicides had no effect. There also appears to be a rate effect with the highest rate of glyphosate (1.68 kg-ai/ha) and dicamba, compared to the lowest rate (0.43 kg-a/ha). 53

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The effect of PGR herbicides with imazapyr was not observed at the 2 lowest rates (0.14 and 0.28 kg-ai/ha) (Table 3-10). The highest rate of imazapyr (0.56 kg-ai/ha) with 2,4-D provided the most control, 75%. The remaining PGR herbicides had no effect on the level of control provided by imazapyr at that rate. Shoot regrowth. There was a significant (p < 0.05) three-way interaction among growth regulator, herbicide, and herbicide rate for the visual evaluation (Table 3-9). Plant growth regulating herbicides applied alone did not differ from the untreated controls (Table 3-11). In fact, only 4 treatments overall differed from these untreated plants, glyphosate at 0.84 kg-ai/ha with dicamba or quinclorac, and imazapyr at 0.56 kg-ai/ha with quinclorac, all increasing the shoot regrowth biomass. The only treatment that decreased shoot biomass compared to the untreated controls was imazapyr at the highest rate (0.56 kg-ai/ha) with 2,4-D. This treatment also yielded less shoot regrowth compared to 2,4-D with the lowest rate of imazapyr. Glyphosate treatments (0.84 kg-ai/ha) with dicamba or quinclorac increased shoot regrowth compared to when they were applied with the lowest and highest glyphosate rates (0.14 and 1.68 kg-ai/ha). However, dicamba with glyphosate at 0.43 kg-ai/ha did not differ from either of the 2 higher rates. By adding glyphosate or imazapyr to the PGR herbicides, the level of control did not differ from the PGR herbicides alone, with the exception of 2,4-D and imazapyr at 0.56 kg-ai/ha. Rhizome biomass. There was no significant (p < 0.05) interaction among variables. (Table 3-9). Also, no treatments reduced rhizome biomass compared to the untreated control (Table 3-12). Experiment two Overall model variance for experiment 2 parameters, including visual evaluation, shoot regrowth biomass and rhizome/root biomass are listed in Table 3-13. 54

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Visual evaluation. There was a significant (p < 0.05) two-way interaction with growth regulator and herbicide rate, but no three-way interaction (Table 3-13). The variable herbicide was not significant. All treatments in this experiment did not differ from control provided by the untreated plants (Table 3-14). The effect of the PGR herbicides was not observed for the 2 highest rates of glyphosate (0.84 and 1.68 kg-ai/ha) or with imazapyr at 0.56 kg-ai/ha. Dicamba with glyphosate (0.43 kg-ai/ha) provided almost 75% control, and was higher in comparison to imazapyr alone, 20%. The greatest level of control observed with imazapyr at 0.14 kg-ai/ha occurred with 2,4-D, dicamba, and triclopyr. Control with imazapyr at 0.28 kg-ai/ha was greatest with dicamba or triclopyr compared to quinclorac at this rate, but these treatments did not differ from imazapyr alone. Shoot regrowth. There was a high level of variability within experiment 2, resulting in no differences among treatments (Table 3-15) Also, no treatments reduced shoot regrowth compared to the untreated control (Table 3-14). Rhizome biomass. There was a high level of variability within experiment 2, resulting in no differences among treatments (Table 3-15). Also, no treatments reduced rhizome biomass compared to the untreated control (Table 3-16). Discussion Acceptable control is defined as having > 80% reduction in rhizome mass 2 years after treatment, on a similar rhizomatous invasive plant, cogongrass (Willard et al. 1996). This level of control can best be achieved on torpedograss if the management method targets the rhizomes and all viable tillers (Sutton 1996, Smith et al. 1999). In this experiment, the rhizomes were targeted using PGR herbicides and either glyphosate or imazapyr. Only one treatment, diflufenzopyr applied tank-mixed with imazapyr (0.56 kg-ai/ha), provided consistent reduction in rhizome biomass compared to imazapyr alone. However, overall lack of consistent distinction in rhizome 55

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dry weight for the diflufenzopyr timing experiment and the growth regulator experiment leads to a closer examination of the visual evaluation and the shoot regrowth dry weight. Thus, acceptable control, in this study, is defined as > 80% injury or visual reduction, 8 weeks after initial treatment. In the timing study, acceptable control was not achieved, regardless of treatment. However, shoot regrowth decreased when diflufenzopyr was applied 3 days before glyphosate (0.43 kg-ai/ha) for experiment 1 when compared to glyphosate alone. This treatment also reduced rhizome biomass. Overall, however, rhizome data indicate that rhizome biomass was reduced more often with glyphosate or imazapyr treatments tank-mixed with diflufenzopyr in either study. Findings by Ketchersid and Senseman (1998) suggested that diflufenzopyr was more phytotoxic to broadleaf plants when applied 3 days before a dicamba application. While this was true for one treatment that decreased shoot regrowth, rhizome data are not consistent with these findings. These differing results may be due to different target weeds; Ketchersid and Senseman (1998) targeted broadleaf weeds, whereas this experiment targeted torpedograss, a grass. Differing results may also be due to different diflufenzopyr tank-mixes. Acceptable control was also not achieved in the growth regulator experiment and results were inconsistent. Similar to the visual evaluation data, shoot regrowth and rhizome dry weight patterns were inconsistent. Also observed with the PGR herbicide treatment was the overall lack of control that was achieved using quinclorac; a registered herbicide for torpedograss in turf grass (Anonymous 2006). Quinclorac when applied with glyphosate (0.84 kg-ai/ha) in experiment 1, actually increased shoot regrowth compared to the highest and the lowest rates. Although not documented with glyphosate, an increase in shoot regrowth by quinclorac alone was also observed by Busey (2003), who indicated that the torpedograss canopy increased after 56

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the initial reduction by quinclorac in a multi-application treatment. Several studies indicate that multiple applications are necessary to achieve acceptable control (McCarty et al. 1993, Busey 2003). McCarty et al. (1993) concluded that quinclorac applications at 2.2 kg-ai/ha followed by 1.1 kg-ai/ha 3 and 6 weeks after initial treatment (WAT) could control torpedograss (85-90% control) for a short time, 7-10 WAIT. Busey (2003) found 4 applications at 0.42 kg-ai/ha per year for 2 years reduced torpedograss dry weight 80%. While this study did not provide long term results, it did provide initial expectations within a short period of time. The advantage of adding/combining PGR herbicides to glyphosate or imazapyr was not observed. The overall inconsistencies may be due to a decrease in translocation or general inconsistencies with the PGR herbicides. Inconsistencies from this study are readdressed in the field study, where results are indicative of real-world situations. Table 3-1. Overall model variance for the visual evaluation, shoot regrowth biomass, and rhizome biomass 8 weeks after initial treatment in the torpedograss diflufenzopyr timing Experiment 1. Variables Visual evaluation p-value Shoot regrowth p-value Rhizome p-value ExperimentP1P < 0.0001 < 0.0001 < 0.0001 Timing 0.2910 0.0130 0.0096 Herbicide 0.4024 0.3816 0.0261 Timing*herbicide 0.7330 0.2055 0.2659 Rate 0.4031 0.1103 0.3833 Timing*herbicide rate 0.3731 0.9476 0.8039 Herbicide* herbicide rate 0.1263 0.0354 0.0469 Timing*herbicide* herbicide rate 0.0130 0.1332 0.6624 Rep 0.7698 0.9323 0.6630 P1PExperiment comparison between experiment 1 and experiment 2 for the torpedograss diflufenzopyr study. 57

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Table 3-2. Percent control of torpedograss regrowth 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 1. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56 % Control Absent 40 26P1P 45 26 18 22 38 20 23 26 30 16 3 days prior 50 0 10 8 13 12 20 24 28 24 43 26 Tank-mix 18 18 23 10 33 12 35 18 43 18 18 16 3 days after 30 8 13 10 15 12 18 12 13 10 40 34 P1PMeans followed by 95% confidence interval. Table 3-3. Torpedograss shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 1. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56 Grams/pot Absent 0.5 0.2 0.6 0.4 0.8 0.2 0.8 0.2 1.0 0.6 0.7 0.2 3 days prior 0.5 0.0 1.0 0.2 0.9 0.0 0.9 0.4 0.9 0.4 0.6 0.4 Tank-mix 0.7 0.2 0.8 0.2 0.6 0.2 0.5 0.1 0.4 0.2 0.7 0.2 3 days after 0.7 0.2 1.2 0.2 1.2 0.2 1.0 0.4 0.9 0.2 0.7 0.2 P1PMeans followed by 95% confidence interval. Table 3-4. Torpedograss rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 1. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56 Grams/pot Absent 2.5 0.0 4.4 0.6 4.2 0.6 5.3 2.2 1.0 0.6 4.5 1.0 3 days prior 4.5 0.8 6.5 2.4 0.9 0.0 5.3 2.0 4.5 0.8 4.0 1.4 Tank-mix 3.5 0.6 5.1 3.6 2.8 0.8 2.3 0.4 3.8 2.2 2.5 0.6 3 days after 6.3 1.6 6.4 1.6 9.3 3.0 6.3 4.8 4.1 1.2 3.0 1.6 P1PMeans followed by 95% confidence interval. 58

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Table 3-5. Overall model variance for the visual evaluation, shoot regrowth biomass, and rhizome biomass 8 weeks after initial treatment in the torpedograss diflufenzopyr timing Experiment 2. Variables Visual evaluation p-value Shoot regrowth p-value Rhizome p-value ExperimentP1P < 0.0001 < 0.0001 < 0.0001 Timing 0.5319 0.6704 0.3534 Herbicide 0.2795 0.6669 0.2225 Timing*herbicide 0.5828 0.2604 0.4043 Herbicide rate 0.0190 0.0817 0.2778 Timing*rate 0.5427 0.4561 0.4010 Herbicide*herbicide rate 0.5720 0.2876 0.1203 Timing*herbicide*herbicide rate 0.1708 0.6870 0.2002 Rep 0.5383 0.5026 0.1541 P1PExperiment comparison between experiment 1 and experiment 2 for the torpedograss diflufenzopyr study. Table 3-6. Percent control of torpedograss regrowth 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 2. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56 % Control Absent 15 6 38 30 33 10 25 26 28 22 23 26 3 days prior 40 8 23 16 15 12 20 24 43 30 48 36 Tank-mix 18 24 50 34 23 10 15 6 55 34 23 32 3 days after 18 10 35 20 33 22 28 22 38 10 23 20 P1PMeans followed by 95% confidence interval. Table 3-7. Torpedograss shoot regrowth (grams/pot) 8 weeks after treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 2. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56 Grams/pot Absent 0.9 0.2 0.6 0.4 0.6 0.2 1.2 1.0 0.9 1.0 0.9 0.6 3 days prior 0.4 0.0 0.8 0.4 1.1 0.4 1.0 0.6 0.7 0.6 0.4 0.6 Tank-mix 1.2 0.6 0.4 0.2 0.8 0.6 0.9 0.2 0.4 0.6 0.2 0.2 3 days after 0.8 0.6 0.6 0.4 1.0 1.0 0.7 0.8 0.4 0.2 0.7 0.6 P1PMeans followed by 95% confidence interval. 59

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Table 3-8. Torpedograss rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in Experiment 2. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56 Grams/pot Absent 5.5 0.6 4.2 2.6 4.0 1.0 5.2 2.8 5.7 2.0 4.7 0.6 3 days prior 2.1 0.8 4.6 2.6 5.9 2.2 6.1 5.2 6.2 5.2 2.5 2.0 Tank-mix 6.3 2.8 1.7 1.2 3.0 1.8 4.3 2.8 4.2 3.2 2.3 1.2 3 days after 4.5 3.0 3.5 2.4 6.0 4.8 5.0 5.0 1.7 0.4 2.5 1.4 P1PMeans followed by 95% confidence interval. Table 3-9. Overall model variance for the visual evaluation, shoot regrowth biomass, and rhizome biomass 8 weeks after initial treatment in the torpedograss growth regulator Experiment 1. Variables Visual evaluation p-value Shoot regrowth p-value Rhizome p-value ExperimentP1P 0.0002 < 0.0001 < 0.0001 Growth regulator 0.0210 0.0578 0.2589 Herbicide 0.0714 0.2558 0.0589 Growth regulator*herbicide 0.0638 0.8696 0.7799 Herbicide rate 0.3293 0.0578 0.0589 Growth regulator*herbicide rate 0.0171 0.0132 0.3582 Herbicide*herbicide rate 0.7065 0.1877 0.0523 Growth regulator *herbicide*herbicide rate 0.0255 0.0007 0.0691 Rep 0.6966 0.5949 0.0948 P1PExperiment comparison between experiment 1 and experiment 2 for the torpedograss growth regulator study. Table 3-10. Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in Experiment 1. Glyphosate (kg-ai/ha)P1P Imazapyr (kg-ai/ha) Growth regulator ControlP1P 0.43 0.84 1.68 0.14 0.28 0.56 % Control Absent 0 0P2P 25 10 38 38 25 26 33 18 20 8 28 6 2,4-D 15 12 25 6 35 32 25 12 13 12 45 22 75 10 Dicamba 35 36 18 18 8 6 35 12 22 8 17 6 33 12 Quinclorac 18 12 25 12 8 10 20 8 30 14 25 18 8 10 Triclopyr 30 12 28 12 35 10 28 20 38 26 28 32 33 16 P1PGrowth regulating herbicides applied alone or in the absence of glyphosate or imazapyr.P 2PMeans followed by 95% confidence interval. 60

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Table 3-11. Torpedograss shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in Experiment 1. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Growth regulator ControlP1P 0.43 0.84 1.68 0.14 0.28 0.56 Grams/pot Absent 0.8 0.4P2P 1.1 0.2 1.3 1.4 1.2 0.6 0.6 0.2 1.2 0.4 1.3 0.8 2,4-D 1.3 0.2 1.0 0.4 1.2 0.8 1.3 0.6 2.2 1.0 0.8 0.6 0.3 0.4 Dicamba 1.0 0.8 1.6 0.4 2.2 0.6 0.9 0.2 1.0 0.2 1.3 0.6 0.9 0.4 Quinclorac 1.4 0.2 1.0 0.4 2.5 1.0 1.0 0.2 1.1 0.8 1.4 0.6 1.8 0.4 Triclopyr 1.1 0.4 1.0 0.4 0.9 0.2 1.3 1.0 0.9 0.6 1.3 0.8 0.8 0.2 P1PGrowth regulating herbicides applied alone or in the absence of glyphosate or imazapyr.P 2PMeans followed by 95% confidence interval. Table 3-12. Torpedograss rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in Experiment 1. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Growth regulator ControlP1P 0.43 0.84 1.68 0.14 0.28 0.56 Grams/pot Absent 6.7 2.6P2P 8.1 2.4 7.7 8.2 2.6 0.4 5.2 3.6 7.3 3.2 6.4 3.2 2,4-D 9.1 2.6 6.8 1.4 5.8 3.2 4.8 1.0P P 10.0 3.2 7.9 4.4 4.5 1.2 Dicamba 6.7 4.2 8.4 2.0 8.8 0.4 3.2 1.0 6.7 26 7.7 2.0 5.4 2.0 Quinclorac 8.9 5.4 6.0 1.8 9.7 3.8 3.2 4.0 5.2 1.0 7.3 1.6 9.2 1.8 Triclopyr 7.9 2.8 5.9 3.0 5.2 0.8 4.8 2.0 3.6 1.0 7.2 3.6 4.0 1.4 P1PGrowth regulating herbicides applied alone or in the absence of glyphosate or imazapyr.P 2PMeans followed by 95% confidence interval. 61

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Table 3-13. Overall model variance for the visual evaluation, shoot regrowth biomass, and rhizome biomass 8 weeks after initial treatment in the torpedograss growth regulator Experiment 2. Variables Visual evaluation p-value Shoot regrowth p-value Rhizome p-value ExperimentP1P 0.0002 < 0.0001 < 0.0001 Growth regulator 0.0036 0.1444 0.4510 Herbicide 0.4440 0.9845 0.4730 Growth regulator*herbicide 0.7152 0.8329 0.5798 Herbicide rate 0.2019 0.5166 0.3138 Growth regulator*herbicide rate 0.0168 0.2622 0.4209 Herbicide*herbicide rate 0.1257 0.3600 0.5778 Growth regulator *herbicide*herbicide rate 0.5232 0.2622 0.8764 Rep 0.9979 0.5362 0.6994 P1PExperiment comparison between experiment 1 and experiment 2 for the torpedograss growth regulator study. Table 3-14. Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in Experiment 2. Glyphosate (kg-ai/ha)P1P Imazapyr (kg-ai/ha) Growth regulator ControlP1P 0.43 0.84 1.68 0.14 0.28 0.56 % Control Absent 18 22P2P 20 16 33 12 18 10 20 8 43 18 28 18 2,4-D 43 24 50 14 23 10 33 6 67 30 28 12 23 10 Dicamba 33 26 73 26 33 10 45 26 45 26 53 20 48 18 Quinclorac 20 18 35 34 28 24 50 36 20 12 25 6 33 22 Triclopyr 35 26 35 18 15 12 50 24 38 30 40 8 35 20 P1PGrowth regulating herbicides applied alone or in the absence of glyphosate or imazapyr.P 2PMeans followed by 95% confidence interval. 62

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Table 3-15. Torpedograss shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in Experiment 2. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Growth regulator ControlP1P 0.43 0.84 1.68 0.14 0.28 0.56 Grams/pot Absent 0.6 0.4P1P 0.9 0.4 0.9 0.6 0.9 0.4 1.3 0.8 0.6 0.4 1.1 0.6 2,4-D 0.6 0.4 0.4 0.4P P 1.1 0.8 0.6 0.2 0.6 0.6 0.9 0.6 0.9 0.2 Dicamba 0.5 0.4 0.2 0.4 0.8 0.6 0.6 0.6 0.5 0.4 0.4 0.2 0.4 0.2 Quinclorac 1.2 0.8 1.1 0.8 0.7 0.4 0.7 1.2 0.7 0.2 0.8 0.4 0.6 0.4 Triclopyr 0.8 0.6 1.1 0.8 0.7 0.2 0.4 0.4 1.4 1.6 0.6 0.2 0.5 0.2 P1PGrowth regulating herbicides applied alone or in the absence of glyphosate or imazapyr.P 2PMeans followed by 95% confidence interval. Table 3-16. Torpedograss rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in Experiment 2. Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha) Growth regulator ControlP1P 0.43 0.84 1.68 0.14 0.28 0.56 Grams/pot Absent 3.7 3.2P2P 5.4 3.6 5.0 2.4 3.8 1.4 6.2 4.0 4.0 2.6 8.2 7.6 2,4-D 3.8 2.0 5.3 3.4 7.5 6.0 2.2 1.4 2.8 3.6 4.3 2.4 3.3 3.0 Dicamba 6.8 5.4 1.2 1.2 3.7 1.8 2.6 2.6 3.1 2.4 4.3 1.4 1.9 0.8 Quinclorac 5.0 3.2 4.4 2.8 4.2 2.2 3.1 2.2 3.5 1.4 4.2 2.6 3.8 1.8 Triclopyr 7.1 6.6 5.0 2.6 3.8 1.8 1.6 1.0 12.1 19.8 4.7 3.6 3.4 1.8 P1PGrowth regulating herbicides applied alone or in the absence of glyphosate or imazapyr.P 2PMeans followed by 95% confidence interval. 63

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CHAPTER 4 EVALUATION OF GROWTH REGULATOR HERBICIDES FOR IMPROVED CONTROL OF COGONGRASS Introduction The state of Florida has been a world leader in the phosphate mine industry since the early 1900s (El-Midany 2004, FIPR 2004a). Extensive mining leads to 4,000 to 6,000 acres of disturbed land annually, which is often exploited by invasive species, such as cogongrass [Imperata cylindrica (L.) Beauv.] (FIPR 2004b, Ewel 1986). Cogongrass, an invasive perennial grass, appears on multiple state noxious weed lists, as well as the federal list (Dickens 1974, Holm et al. 1977, USDA 2005a, 2005b). One of the major reasons that cogongrass is such a successful invader is due to its extensive rhizome system. These rhizomes comprise greater than 60% of the entire plants biomass (Sajise 1976). Eussen (1979) reported eleven weeks after initial rhizome growth, the rhizome mass may occupy an area as large as 4mP2P. In a mature stand, cogongrass can develop as many as 350 shoots from its rhizome mass in a 6-week period (Eussen 1979).Terry et al. (1997) suggested that cogongrass may even sacrifice leaf production to maintain a healthy rhizome base. Complete control of cogongrass requires total removal of all viable tillers and rhizomes (Tanner et al. 1992, Willard et al. 1997). The current best management practices for cogongrass, regardless of method or integration of methods, cannot effectively control the plant to the point of complete eradication without tremendous and often unfeasible means (Willard et al. 1997). A number of herbicidal studies have been performed on cogongrass (Dickens and Buchanan 1975). Herbicide applications to cogongrass are often difficult due to the high level of rhizomes compared to leaves present (Coile and Shilling 1993). Those herbicides that have provided the best results with the fewest adverse effects include glyphosate [N-(phosphonomethyl) glycine], imazapyr (2-[4,5-dihydro-4-methyl-4-(1-methylethyl)-5-oxo-1-H64

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imidazol-2-yl]-3-pyridinecarboxylic acid), and dalapon (2,2-Dichloropropionic acid, no longer registered) (Willard et al. 1997). Willard et al. (1996) reported that glyphosate and imazapyr can control cogongrass better than dalapon in the absence of mechanical treatments. Glyphosate produces rapid cogongrass defoliation, with no soil residual activity (Townsend and Butler 1990). Imazapyr is slower acting, but residual soil activity (25 to 142 day half life) provides better long term control (Johnson et al. 1997, Willard et al. 1997, WSSA 2002). Applications of 3.4 kg-ai/ha of glyphosate or 0.8 kg-ai/ha of imazapyr provided 60 and 70% cogongrass control, respectively. However, when these herbicides were sequentially applied, control ranged from 87 to 98% control 19 months after initial treatment regardless of application order (Willard et al. 1997). There have been several reports that glyphosate or imazapyr herbicide applications in the fall provide increased control (Gaffney 1996, Johnson et al. 1999). Gaffney (1996) also indicated > 20% more control was achieved 1 year after treatment with the same herbicides and rates in a fall application versus a spring or summer application. Although seed spread is a concern, the biggest hurdle in developing a viable management strategy for cogongrass is control of rhizomes. Rhizomes exhibit apical dominance which suppresses the growth of shoots from subapical nodes (Cline 1994). Studies with auxinic hormones suggest that auxins play a role in apical dominance in cogongrass, possibly causing unequal distribution of carbohydrates and, consequently, systemic herbicides in the rhizomes (Gaffney and Shilling 1995, Gaffney 1996). Gaffney (1996) reported that cogongrass rhizomes with apices removed produced 31% more shoots than rhizomes with intact apices. Therefore, disruption of normal auxin levels in rhizome grasses may release stored carbohydrates and encourage new shoot production of otherwise dormant buds (Cline 1994, English 1998). This 65

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generally occurs with physical injury, but it has been hypothesized that growth regulator herbicides could cause this effect as well. By disrupting apical dominance, systemic herbicides may be distributed more evenly and potentially provide more complete control. Herbicides in the growth regulator classification interfere with growth hormone functions and have similar modes of action and selectivity (Anderson 1996). Although the true mode of action for many of these herbicides is unknown, it is speculated some have auxin-like properties that mimic auxins in an unregulated fashion within plant tissues (Anderson 1996, Lym and Deibert 2005). Other growth regulating herbicides such as diflufenzopyr inhibit the transport of auxins (Grossman et al. 2002, WSSA 2002). Limited information is available on the use of PGR herbicides such as triclopyr, dicamba, 2,4-D, and diflufenzopyr and quinclorac for cogongrass control. Preliminary studies suggest that certain PGR herbicides, specifically 2,4-D and diflufenzopyr (1.12 and 0.28 kg-ai/ha respectively) when tank-mixed with imazapyr (0.56 kg-ai/ha) may provide acceptable control of regrowth (> 85%) for at least 8 weeks after initial treatment (WAIT) (Ketterer et al. 2006, Ketterer et al. 2007). These results, although informative, do not clarify how well these treatments will work in the field. If apical dominance can be disrupted using these PGR herbicides and thus stimulate shoot growth, then perhaps an initial application of PGR herbicides followed by a glyphosate or imazapyr treatment would provide better herbicide efficacy. The objective of this study was to evaluate the effect of several growth regulating herbicides for improved efficacy of glyphosate and imazapyr for cogongrass control. Pre-treatment interval and time of year were also evaluated within the context of this objective. This timing component was included in this study to evaluate whether a pre-conditioning period is needed (to stimulate axillary bud break and sprouting). 66

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Materials and Methods Methodology Field studies were conducted at Tenoroc Fish Management Area in Polk County, Florida. This site was originally a phosphate mine, but is currently infested with dense and mature stands of cogongrass. The entire area was burned in February of 2006. Studies were initiated in spring (March) 2006, and herbicide treatments were applied 3 times throughout the year; experiment 1 spring (March), experiment 2 summer (June), experiment 3 fall (September). All herbicides were applied using a COB2B pressurized sprayer calibrated to deliver 187 L/ha. A non-ionic surfactant (0.25% v/v) was added with each herbicide. Plant growth regulating herbicide treatments included diflufenzopyr (0.28 kg-ai/ha), triclopyr (0.42 kg-ai/ha), quinclorac (1.40 kg-ai/ha), dicamba (0.56 kg-ai/ha) and 2,4-D (1.12 kg-ai/ha). Within each growth regulator herbicide treatment, imazapyr (0.84 kg-ai/ha) or glyphosate (3.36 kg-ai/ha) herbicides were applied one time at 4 timing intervals. These intervals included 0 (same day), 1, 2, or 3 months after the initial PGR herbicide treatment. The experiment was a split plot design, with the main effect being PGR herbicide treatment and herbicide and application timing being subplot effects. Visual evaluations were taken 3, 6, and 9 months after the initial PGR herbicide application and based on the following scale: 0 = no control; 100 = complete control. Statistical Analysis The data were analyzed using proc GLM program in SAS 9.1. Treatments were regarded as split-plot occurring within growth regulating herbicide. Models for the independent variables (experiment, growth regulator, herbicide, and month of application) were determined using the dependent variables (3, 6, and 9 month evaluations). Means and least significant difference (LSD) were determined for the dependent variables according to the growth regulator, the herbicide, and the month of herbicide application. 67

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Results Spring Experiment Three month evaluation. There was a significant (p < 0.05) two-way interaction with herbicide and month (Table 4-1). Averaged across all PGR herbicides, glyphosate and imazapyr treatments did not differ within month of herbicide application for the 3 month evaluation after the initial PGR herbicide treatments (Table 4-2). When glyphosate was applied 3 months after the initial PGR herbicides, less control was observed compared to the remaining herbicide application months. Imazapyr applied on the same day (0 month) as the PGR herbicides provided more control compared to when it was applied 2 or 3 months after. There was a significant (p < 0.05) two-way interaction with month and growth regulating herbicide (Table 4-1). When treatments were applied on the same day (0 month) as the PGR herbicides, 2,4-D provided the least control, when averaged across herbicide (Table 4-3). Dicamba with glyphosate or imazapyr at the 0 month application provided 84% control, but did not differ from quinclorac or triclopyr treatments. When glyphosate or imazapyr were applied 1 month after the initial PGR herbicides dicamba, diflufenzopyr, and triclopyr treatments provided the most control. Varying levels of control were observed when glyphosate or imazapyr were applied 2 months after the PGR herbicides, and no treatment exceeded 60% control. When glyphosate or imazapyr were applied 3 months after any PGR herbicides < 35% control was observed. Six month evaluation. There was a significant (p < 0.05) two-way interaction with herbicide and month (Table 4-1). Averaged across PGR herbicides, control within glyphosate for the 6 month evaluation in the spring experiment was lower for the 0 month herbicide timing (same day application) compared to when glyphosate was applied 2 or 3 months after the PGR herbicides (Table 4-4). Glyphosate control did not exceed 65% when it was applied the same day 68

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as (0 month) or 1 month after the initial PGR herbicide treatment. Imazapyr treatments did not differ across months, providing > 94% control. There was a significant (p < 0.05) two-way interaction with herbicide and growth regulator (Table 4-1). Imazapyr control was greater when mixed with 2,4-D, diflufenzopyr, and quinclorac, compared to glyphosate, when averaged across month of application. (Table 4-5). Glyphosate control with dicamba or triclopyr was greater in comparison to 2,4-D but did not differ from the remaining PGR herbicides. Imazapyr treatments provided > 93% control with any PGR herbicide. There was a significant (p < 0.05) two-way interaction with month and growth regulating herbicide (Table 4-1). Averaged across herbicides, when glyphosate or imazapyr was applied 2 or 3 months after the initial PGR herbicides, > 80% control was observed with any PGR herbicide. (Table 4-6). Control was greatest with 2,4-D when glyphosate or imazapyr were applied 1, 2, and 3 months after 2,4-D. When glyphosate or imazapyr were applied 0, 1, or 2 months after dicamba, the level of control was higher compare to when glyphosate or imazapyr was applied 3 months after dicamba. Control was greatest for diflufenzopyr, quinclorac, and triclopyr when glyphosate or imazapyr were applied 2 or 3 months after. Nine month evaluation. There was a significant (p < 0.05) two-way interaction with herbicide and month (Table 4-1). Across all PGR herbicides, imazapyr provided more control than glyphosate when applied 0, 1, and 2 months after PGR herbicides for the 9 month evaluation on the spring experiment (Table 4-7). However, no difference was observed when these herbicides were applied 3 months after the initial PGR herbicides. When glyphosate was applied 2 and 3 months after the PGR herbicides, control was greater compared to the same day 69

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(0 month) treatment. Imazapyr provided > 89% control when applied at any month of application. There was a significant (p < 0.05) two-way interaction with herbicide by growth regulator (Table 4-1). Averaged across herbicide application months, imazapyr provided more control with 2,4-D compared to glyphosate (Table 4-9). The remainder of the glyphosate/imazapyr treatments did not differ within PGR herbicides. Dicamba and triclopyr provided more control compared to 2,4-D or diflufenzopyr, when mixed with glyphosate. Imazapyr treatments provided > 86% control with any PGR herbicide. There was a significant (p < 0.05) two-way interaction with month and growth regulating herbicide (Table 4-1). Averaged across glyphosate/imazapyr treatments, the best control was observed when glyphosate or imazapyr were applied 2 and 3 months after 2,4-D, dicamba, and triclopyr (Table 4-9). However, dicamba treatments did not differ across month of herbicide application. When glyphosate or imazapyr was applied 3 months after diflufenzopyr, control was greater compared to the remaining herbicide application months. Quinclorac provided the most control when glyphosate or imazapyr was applied 2 months after, compared to the remaining application months. Summer Experiment Three month evaluation. There was no significant (p < 0.05) interaction (Table 4-1). However, the variables month and growth regulator were significant, while herbicide was not. Averaged across glyphosate or imazapyr and month of herbicide application, the greatest control was observed with 2,4-D, dicamba, and diflufenzopyr for the 3 month evaluation on the summer experiment (Table 4-11). However, diflufenzopyr did not differ from the remaining PGR herbicides treatments. Averaged across PGR herbicides and glyphosate or imazapyr, when 70

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herbicides were applied on the same day (0 month) as the PGR herbicides > 92% was observed (Table 4-12). The 3 month herbicide application provided almost no control. Six month evaluation. There was a significant (p < 0.05) two-way interaction with herbicide and month, but no three-way interaction (Table 4-10). Across PGR herbicides, imazapyr provided more control when applied on the same day (0 month) as the PGR herbicide, for the 6 month evaluation on the summer experiment compared to glyphosate (Table 4-13). However, glyphosate yielded more control when applied 3 months after PGR herbicide. This glyphosate treatment provided greater control than when applied at the 0 or 1 month application. When imazapyr was applied 0, 1, or 2 months after the initial PGR herbicides control was > 89%. Growth regulator was a significant (p < 0.05) variable (Table 4-10). Greater than 75% control was observed for all of the PGR herbicide treatments (Table 4-14). Dicamba and 2,4-D provided greater control compared to quinclorac or triclopyr. Fall Experiment Three month evaluation. There was no significant (p < 0.05) interaction (Table 4-15). However, the variables month and growth regulator were significant when examined alone (Table 4-15). The PGR herbicide treatments, averaged across herbicide and month of herbicide application, failed to provide > 70% control in the 3 month evaluation on the fall experiment (Table 4-16). Dicamba, and 2,4-D provided the greatest level of control compared to the remaining PGR herbicides. When averaged across glyphosate or imazapyr and PGR herbicides, the 0 and 1 month herbicide application timing provided greater control compared to the 2 and 3 month herbicide application (Table 4-17). When glyphosate or imazapyr applications occurred 2 and 3 months after the initial PGR herbicide application, control was < 50%. 71

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Discussion Acceptable cogongrass control is defined as having > 80% reduction in rhizome biomass 2 years after treatment (Willard et al. 1996). This level of control can best be achieved if the management method targets the rhizomes and all viable tillers (Tanner et al. 1992, Willard et al. 1997). In this experiment, the rhizomes were targeted using growth regulator herbicides and either glyphosate or imazapyr. However, rhizome data were not examined and acceptable control, in this study, is defined as > 80% injury or visual reduction, 3, 6, or 9 months after initial treatment (MAT). The evaluation 3 months after initial treatment (MAT) did not accurately reflect data trends. Glyphosate or imazapyr treatments applied 3 months after the initial PGR herbicides occurred just minutes before the evaluation. Thus, results may appear biased in reflecting that the 0 month (same day application as the PGR herbicides) treatments provided more control compared to the 3 month application when evaluated 3 MAT, when, in fact, the 0 month treatments were allowed the necessary interval between application and injury symptoms. The interval was not long enough to observe these symptoms when glyphosate or imazapyr were applied 3 months after PGR herbicides. There does appear to be a critical time frame between application of any PGR herbicide followed by either glyphosate or imazapyr. If the PGR herbicides are applied first and imazapyr application follows either the same day (0 month) or 1 or 2 months after, cogongrass control can be > 89% starting at 6 MAT and continuing through 9 MAT. For glyphosate, > 80% control at 6 and 9 MAT occurred when the herbicide was applied 2 or 3 month after the PGR herbicides. Another trend was the consistent control observed with imazapyr and any PGR herbicide, > 85% at 6 and 9 months. Studies by Ketterer et al. (2006 and 2007) indicated that one would expect similar results on cogongrass with 2,4-D or diflufenzopyr and imazapyr in the 72

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greenhouse. The most consistent control with glyphosate occurred with triclopyr and dicamba treatments, approximately 85% control for triclopyr and approximately 80% control with dicamba 6 and 9 MAT. These findings compliment observations by Flint and Barrett (1989). A study on johnsongrass (Sorghum halepense L.) indicated that glyphosate and dicamba (0.28, 0.49, and 0.56 kg-ai/ha) had antagonistic effects on shoot production at low rates of glyphosate, 0.28 and 0.56 kg-ai/ha. The chemicals then became synergistic when glyphosate rates increased above 0.56 kg-ai/ha (Flint and Barrett 1989). Triclopyr has been documented to have synergistic effects with other herbicides such as clopyralid (Bovey and Whisenat 1992). However, no such documentation occurs on the synergism of triclopyr and glyphosate. This study was replicated in the spring, summer, and fall. Previous studies indicate that herbicide applications in the fall tend to result in greater efficacy compared to spring treatments (> 20% more control, 12 months after treatment) for both glyphosate and imazapyr as they are actively translocated with the photosynthates to the rhizomes (Tanner et al. 1992, Gaffney 1996, Johnson et al. 1997). It can be expected that glyphosate (2.24 kg-ai/ha) or imazapyr (0.84 kg-ai/ha) treatments on cogongrass will provide approximately 70-80% control up to 1 year after treatment when applied in the fall. Similar levels of control were observed 9 MAT for the spring study. The inclusion of PGR herbicides with glyphosate or imazapyr treatment could result in more complete control regardless of the season. Although the results appear promising for cogongrass control, the issue of long-term control has yet to be established as the data presented are only indicative of 9 month ratings after only the spring treatment. The majority of experimental plots with 100% control were either bare ground or covered by volunteer weeds such as hairy indigo (TIndigofera hirsutaT L.) and passion flower (Passiflora incarnate L.). Bare ground plots are a cause for concern if the below-ground 73

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rhizomes still prove viable or cogongrass seeds are present in the seed-bank. Burke and Grime (1996) found that open niches such as bare ground correlate with an influx of invasive species. However, high densities of volunteer weeds may help suppress cogongrass development. For example, landholders are encouraged to use legumes such as velvetbean (Mucuna pruriens var. utilis) in areas where cogongrass is problematic (Akobundu et al. 2000, Versteeg and Koudokpon 1990). Leguminous cover crops seem to be the most effective competitor to cogongrass due to nitrogen fixation and soil enhancement from the plant (Ibewiro et al. 2000). The problem with cultural control is that some cover species may require 2-5 years to become effective in slowing or reducing cogongrass (Akobundu et al. 2000). However, in this study, cover species were not directly planted after treatment. Natural seed banks within the soil contributed the volunteer species which were able to recover and shade out cogongrass within 3-6 months. Although there is no supporting data, it has been suggested that the leguminous hairy indigo may be imazapyr resistant (Conway Duever 2003) and shows promise of future control as legumes have been recommended as cover crops (Ibewiro et al. 2000). Table 4-1. Overall model variance for the control evaluations 3, 6, and 9 months after treatment (MAT) in the cogongrass spring field experiment. Variables 3 MAT 6 MAT 9 MAT Rep 0.0016 0.5394 0.7280 Herbicide 0.0310 < 0.0001 < 0.0001 Month < 0.0001 < 0.0001 < 0.0001 Herbicide*month 0.0073 < 0.0001 < 0.0001 Growth regulator 0.0018 0.0102 0.0089 Herbicide*growth regulator 0.1213 0.0047 0.0215 Month*growth regulator 0.0388 0.0093 0.0186 Herbicide*month*growth regulator 0.4524 0.5393 0.1778 74

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Table 4-2. Averaged across plant growth regulating herbicides, the effect of herbicide and month of application on cogongrass control 3 months after initial plant growth regulating herbicide application for the spring experiment. P1PMeans within month (column) followed by the same symbol are not significantly different Month of herbicide applicationP1P 0 1 2 3 % Control Glyphosate 63*a 65*a 51*a 30*b Imazapyr 80*a 67*ab 54*b 25*c LSD (0.05) = 19. Means within herbicide (row) followed by the same letter are not significantly different LSD (0.05) = 15. Table 4-3. Averaged across herbicides, the effect of plant growth regulating herbicide and month of application on cogongrass control 3 months after initial plant growth regulating herbicide application for the spring experiment. MonthP1P 2,4-DP2P Dicamba Diflufenzopyr Quinclorac Triclopyr % Control 0 53*c 84*a 69*b 76*ab 76*ab 1 58*b 76*a 69*a 56b 70*a 2 48*bc 56ab 60*a 53ab 45bc 3 25a 24a 29a 28a 33a P1PMonth of glyphosate or imazapyr application. P2PMeans within growth regulator (column) followed by the same symbol are not significantly different LSD (0.05) = 17. Means within month (row) followed by the same letter are not significantly different LSD (0.05) = 9. Table 4-4. Averaged across plant growth regulating herbicides, the effect of herbicide and month of application on cogongrass control 6 months after initial plant growth regulating herbicide application for the spring experiment. Month of herbicide applicationP1P 0 1 2 3 % Control Glyphosate 51b 62*ab 87*a 87*a Imazapyr 99*a 95*a 100*a 94*a P1PMeans within month (column) followed by the same symbol are not significantly different LSD (0.05) = 38. Means within herbicide (row) followed by the same letter are not significantly different LSD (0.05) = 30 75

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Table 4-5. Averaged across month of application, the effect of herbicide and growth regulator on cogongrass control 6 months after initial plant growth regulating herbicide application for the spring experiment. 2,4-DP1P Dicamba Diflufenzopyr Quinclorac Triclopyr % Control Glyphosate 57b 86*a 71ab 60ab 82*a Imazapyr 99*a 93*a 99*a 94*a 100*a P1PMeans within growth regulator (column) followed by the same symbol are not significantly different LSD (0.05) = 26. Means within herbicide (row) followed by the same letter are not significantly different LSD (0.05) = 24. Table 4-6. Averaged across herbicide, the effect of growth regulator and month of application on cogongrass control 6 months after initial plant growth regulating herbicide application for the spring experiment. MonthP1P 2,4-DP2P Dicamba Diflufenzopyr Quinclorac Triclopyr % Control 0 51b 94*a 71b 70b 86a 1 80a 89*a 81a 55b 85a 2 91*a 94*a 93*a 96*a 98*a 3 95*a 81b 95*a 86*ab 94*ab P1PMonth of glyphosate or imazapyr application. P2PMeans within growth regulator (column) followed by the same symbol are not significantly different LSD (0.05) = 10. Means within month (row) followed by the same letter are not significantly different LSD (0.05) = 13. Table 4-7. Averaged across plant growth regulating herbicide, the effect of growth regulator and month of application on cogongrass control 9 months after initial plant growth regulating herbicide application for the spring experiment. Month of herbicide applicationP1P 0 1 2 3 % Control Glyphosate 44b 66ab 80a 89*a Imazapyr 97*a 95*a 100*a 89*a P1PMeans within month (column) followed by the same symbol are not significantly different LSD (0.05) = 19. Means within herbicide (row) followed by the same letter are not significantly different LSD (0.05) = 26. Table 4-8. Averaged across month of application, the effect of growth regulator and herbicide on cogongrass control 9 months after initial plant growth regulating herbicide application for the spring experiment. 2,4-DP1P Dicamba Diflufenzopyr Quinclorac Triclopyr % Control Glyphosate 59*b 84*a 59*b 64*ab 82*a Imazapyr 98a 94*a 98*a 86*a 100*a P1PMeans within growth regulator (column) followed by the same symbol are not significantly different LSD (0.05) = 26. Means within herbicide (row) followed by the same letter are not significantly different LSD (0.05) = 22. 76

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Table 4-9. Averaged across herbicides, the effect of growth regulator and month of application on cogongrass control 9 months after initial plant growth regulating herbicide application for the spring experiment. MonthP1P 2,4-DP1P Dicamba Diflufenzopyr Quinclorac Triclopyr % Control 0 50c 91*a 59bc 68b 85a 1 78a 86*a 80ba 75a 81a 2 91*ab 93*a 79b 91*ab 96*a 3 95*ab 85*b 96*ab 70c 100*a P1PMonth of glyphosate or imazapyr application. P2PMeans within growth regulator (column) followed by the same symbol are not significantly different LSD (0.05) = 10. Means within month (row) followed by the same letter are not significantly different LSD (0.05) = 13. Table 4-10. Overall model variance for the control evaluations 3 and 6 months after treatment (MAT) in the cogongrass summer field experiment. Variables 3 MAT 6 MAT Rep 0.5204 0.1111 Herbicide 0.5133 0.1373 Month < 0.0001 0.4485 Herbicide*month 0.8638 < 0.0001 Growth regulator < 0.0001 0.0005 Herbicide*growth regulator 0.6661 0.6892 Month*growth regulator 0.8642 0.7400 Herbicide*month*growth regulator 0.9708 0.1678 Table 4-11. Effect of growth regulator, averaged across herbicide and month of glyphosate or imazapyr application, on cogongrass control 3 months after initial plant growth regulating herbicide application for the summer experiment. Growth regulatorP1P % ControlP1P 2,4-D 66a Dicamba 63a Diflufenzopyr 52ab Quinclorac 47b Triclopyr 47b P1PMeans followed by the same letter are not significantly different LSD (0.05) = 10. 77

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Table 4-12. Effect of month of application, averaged across herbicide and plant growth regulating herbicides, on cogongrass control 3 months after initial plant growth regulating herbicide application for the summer experiment. MonthP1P % ControlP1P 0 92a 1 70b 2 47c 3 11d P1PMonth of glyphosate or imazapyr application. P2PMeans followed by the same letter are not significantly different LSD (0.05) = 7. Table 4-13. Averaged across plant growth regulating herbicides, the effect of herbicide and month of application on cogongrass control 6 months after initial plant growth regulating herbicide application for the summer experiment. Month of herbicide applicationP1P 0 1 2 3 % Control Glyphosate 76b 80*b 84*ab 93*a Imazapyr 99*a 89*a 90*a 72b P1PMeans within month (column) followed by the same symbol are not significantly different LSD (0.05) = 12. Means within herbicide (row) followed by the same letter are not significantly different LSD (0.05) = 10. Table 4-14. Effect of growth regulator, averaged across herbicide and month of glyphosate or imazapyr application, on cogongrass control 6 months after initial plant growth regulating herbicide application for the summer experiment. Growth regulatorP1P % ControlP1P 2,4-D 93a Dicamba 90a Diflufenzopyr 87ab Quinclorac 78b Triclopyr 78b P1PMeans followed by the same letter are not significantly different LSD (0.05) = 9. Table 4-15. Overall model variance for the control evaluation 3 months after treatment (MAT) in the cogongrass fall field experiment. Dependent variables 3 MAT Rep 0.3062 Herbicide 0.3948 Month < 0.0001 Herbicide*month 0.4224 Growth regulator < 0.0001 Herbicide*growth regulator 0.4631 Month*growth regulator 0.6534 Herbicide*month*growth regulator 0.7867 78

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Table 4-16. Effect of growth regulator, averaged across herbicide and month of glyphosate or imazapyr application, on cogongrass control 3 months after initial plant growth regulating herbicide application for the fall experiment. Growth regulatorP1P % ControlP1P 2,4-D 69a Dicamba 68a Diflufenzopyr 48b Quinclorac 46b Triclopyr 30b P1PMeans followed by the same letter are not significantly different LSD (0.05) = 14. Table 4-17. Effect of month of application, averaged across herbicide and plant growth regulating herbicide, on cogongrass control 3 months after initial plant growth regulating herbicide application for the fall experiment. MonthP1P % ControlP2P 0 67a 1 62a 2 44b 3 34b P1PMonth of glyphosate or imazapyr application. P2PMeans followed by the same letter are not significantly different LSD (0.05) = 12. 79

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CHAPTER 5 EVALUATION OF GROWTH REGULATOR HERBICIDES FOR IMPROVED CONTROL OF TORPEDOGRASS Introduction Lake Okeechobee, the second largest closed-system freshwater lake in the United States has a surface area of 1,732 kmP2P and an average depth of 2.7 meters (Jin et al. 1998). There are roughly 40,000 ha of littoral zone in the lake; of which 6,000 ha of native plants have been displaced by torpedograss (Panicum repens L.) (Schardt 1992). The presence of this plant impacts the lakes multi-million dollar sport and recreation fisheries, as the monospecific stands provide poor habitat for fish and water fowl (Hanlon and Langeland 2000). Torpedograss is a serious detriment in Lake Okeechobee, as well as other aquatic systems in Florida and has been ranked by the Florida Department of Environmental Protection as the 2PndP most abundant plant in Florida lakes since 1992 (Schardt 1992, Schardt personal communication, Feb 21, 2007). The presence of torpedograss is additionally problematic in Florida because it interrupts flood control, irrigation and turf production (Shilling and Haller 1989, McCarty et al. 1993). Contributing to this threat are the plants rhizomes. Torpedograss large rhizome system comprises 70 to 90% of the plants biomass (Smith et al. 1999). When fragmented, rhizomes buds can regenerate at a rate of 92 to 96% in temperatures of 20 to 35C (Hossain et al. 2001). New buds are continuously produced along the entire length of the rhizomes indicating weak apical dominance (Wilcut et al. 1988a). Since all of the nodes found on the rhizome system can be viable, complete control of torpedograss requires total removal of all viable tillers and rhizomes (Sutton 1996, Smith et al. 1999). Most management studies on torpedograss come with mixed success, but few have provided 100% long term control (> 12 months) within time constraints and budgets for the average landowner (Manipura and Somaratne 1974, Willard et al. 1998, Smith et al. 1999). 80

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Herbicidal studies have primarily focused on glyphosate and imazapyr (Baird et al. 1983, Shilling and Haller 1989, Willard et al. 1998, Smith et al. 1999, Hanlon and Langeland 2000). Limited control with these herbicides is often attributed to the aquatic habitat of torpedograss where herbicide absorption occurs only on the emergent portion of the plant (Baird et al. 1983, Smith et al. 1999). When using glyphosate only the emergent stems were controlled, but rapid regrowth often occurred from rhizomes and submerged stem segments within a few months (Baird et al. 1983). Smith et al. (1999) concluded that high water levels inhibit foliar interception of glyphosate and control correlated with foliar exposure to water level ratio. To achieve 90% control (5 weeks after initial treatment), a glyphosate application rate of 2.24 kg-ai/ha was needed to be intercepted by at least 40% of the foliage. Lower rates correlated with a higher percentage of foliage cover to achieve similar results (Smith et al. 1999). Imazapyr applications on torpedograss have similar problems with submergence, and in turn, less control (Hanlon and Langeland 2000). Inconsistencies in data presented by Hanlon and Langeland (2000) lead the authors to speculate that fluctuating water depth at different experimental sites could have influenced results. While all experiments began in approximately 0.8m of water, by the end of the experiment, one study site was considered dry while the remaining sites were flooded. Greater than 95% control was observed at the dry site with < 25% control at the flooded sites. The authors also speculated that thatch levels may have contributed to inconsistent control as the amount of torpedograss tissue exposed to the herbicide may be reduced. This reduction may result from thatch blocking the herbicide from hitting the plants (Hanlon and Langeland 2000). While speculating that control with glyphosate or imazapyr is inversely proportional to submerged tissue, considerations to improve herbicide efficacy arise. If torpedograss could be 81

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stimulated to increase shoot production, allowing more of the plant to emerge, then herbicide applications of glyphosate or imazapyr could potentially be more effective. It was speculated that auxin-like herbicides could be used to stimulate shoot production. Herbicides in this classification interfere with growth hormone functions and have similar modes of action and selectivity (Anderson 1996). While the true mode of action of some of these herbicides is unknown, it is speculated that some of these PGR herbicides mimic auxins and may lead to increased sprouting at nodes (e.g. 2,4-D, dicamba, diflufenzopyr, quinclorac) (Anderson 1996, WSSA 2002, Lym and Deibert 2005). Other growth regulating herbicides such as diflufenzopyr inhibit the transport of auxins (Grossman et al. 2002, WSSA 2002). Limited information is available on the use of PGR herbicides such as triclopyr, dicamba, 2,4-D, and diflufenzopyr for torpedograss control. Previous greenhouse data suggest inconsistent control was observed 8 weeks after initial treatment when PGR herbicides were combined with either glyphosate or imazapyr (Ketterer et al. 2007). These results do not clarify how well these treatments will work in the field. The objective of this study was to evaluate the effect of several growth regulating herbicides in conjunction with glyphosate or imazapyr for torpedograss control under field conditions. Materials and Methods Methodology A field study was conducted on the north shore of Lake Okeechobee (27 05.985N, 080 55.680W) on a mature stand of densely populated torpedograss. In this site the torpedograss was roughly 0.5 meters in height with a heavy thatch layer on the ground. The study was initiated in May 2006. Treatments included 5 PGR herbicides (diflufenzopyr 0.28 kg-ai/ha, triclopyr 0.42 kg-ai/ha, quinclorac 1.4 kg-ai/ha, dicamba 0.56 kg-ai/ha, and 2,4-D 1.12 kg-ai/ha) tank-mixed with either glyphosate (3.36 kg-ai/ha) or imazapyr (0.84 kg-ai/ha). Appropriate nonionic 82

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surfactant volume (0.25% v/v) was applied with each treatment. Glyphosate and imazapyr were applied without PGR herbicides for comparison along with an untreated control. All treatments were applied using a backpack sprayer calibrated to deliver 187 L/ha. Efficacies of treatments were visually evaluated as percent control based upon the growth and health of untreated plots (0 = no control, 100 = complete control) at 3, 6, and 9 months after treatment. The experiment was arranged in a completely randomized block design with four replications. Statistical Analysis The data were analyzed using proc GLM program in SAS 9.1. The untreated control was not included in the analyses to assess the impact of the growth regulating herbicides. Models for the independent factors (growth regulator and herbicide) were determined using the dependent variables (3, 6, and 9 month evaluations). Data were presented as means with 95% confidence intervals Results and Discussion Analysis of variance indicated a significant (p < 0.05) two-way interaction with herbicide and growth regulator for the evaluations 3, 6, and 9 months after treatment (MAT) (Table 5-1). Plant growth regulating herbicides had no effect on glyphosate control 3, 6, or 9 MAT (Table 5-2). Glyphosate control never exceeded 60%. Nine MAT, control from quinclorac with glyphosate declined compared to 3 MAT. Greater than 70% control was observed with imazapyr when applied alone or with dicamba, diflufenzopyr, quinclorac, or triclopyr. With the exception of 2,4-D, the PGR herbicides had no effect on the level of torpedograss control observed. Treatments with 2,4-D provided almost no control throughout the experiment, indicating that the two herbicides potentially nullified the effects of the other. Compared to the evaluation 3 MAT, control declined 83

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for most PGR herbicides at 6 MAT. Treatments with diflufenzopyr declined 9 MAT compared to 3 MAT. Possible explanations for the overall lack of control may be attributed to many things. The torpedograss site was not flooded for the duration of the study, excluding theories by Smith et al. (1999) who suggested glyphosate control of torpedograss was related to the proportion of emergent stems to the intercepted herbicide rate. However, there was a thick layer of thatch which Hanlon and Langeland (2000) suggested could possibly contribute to poor control with imazapyr; this may also be a reason for the poor glyphosate control in this study. But approximately 80% of the stem was above the thatch line and since glyphosate lacks soil activity this should have no bearing on control. Imazapyr treatments yielded less than expected control, in general. The residual activity of imazapyr tends to provide lengthy control due to its 25 to 142 day half-life in the soil (WSSA 2002). Poor torpedograss control was also observed with glyphosate and imazapyr with PGR herbicides in greenhouse studies (Ketterer et al. 2007). Therefore, it is possible that torpedograss simply did not respond to the PGR herbicide treatments. Since long term control was not established with this study, further research is warranted. Table 5-1. Overall model variance for the control evaluations 3 and 6 months after treatment (MAT) in the torpedograss field experiment. Variable 3 MAT 6 MAT 9 MAT Herbicide < 0.0001 < 0.0001 0.0004 Growth regulator < 0.0001 0.0022 0.1452 Herbicide*growth regulator < 0.0001 0.0045 0.0029 Rep 0.6192 0.3653 0.1355 84

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Table 5-2. Influence of plant growth regulating herbicides applied with glyphosate and imazapyr for control of torpedograss at 3, 6, and 9 months after treatment (MAT). Glyphosate Imazapyr Growth regulator 3 MAT 6 MAT 9 MAT 3 MAT 6 MAT 9 MAT % Control Absent 34 20P1P 30 14 20 12 73 42 65 34 63 20 2,4-D 50 14 40 24 38 26 0 0 8 6 5 6 Dicamba 53 10 48 28 28 28 93 6 73 10 43 22 Diflufenzopyr 53 10 53 24 43 28 90 8 80 8 55 18 Quinclorac 60 12 38 28 25 12 88 6 70 8 43 18 Triclopyr 45 26 30 14 13 18 93 6 65 20 63 12 P1PMeans followed by 95% confidence interval. 85

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CHAPTER 6 CONCLUSIONS A study was derived to improve glyphosate and imazapyr efficacy using growth regulating herbicides. The growth regulators chosen have auxin-regulating properties (Anderson 1996, Cline 1997, Taiz and Zeiger 2006). By using these growth regulating herbicides to stimulate shoot production, the goal was to provide more complete control by depleting the carbohydrate reserves in the rhizomes as a result of shoot stimulation. It was hypothesized that the combination of plant growth regulating (PGR) herbicides with glyphosate or imazapyr would increase herbicide efficacy in cogongrass and torpedograss. Both greenhouse and field studies were conducted using glyphosate and imazapyr combined in various treatments with the PGR herbicides 2,4-D, dicamba, diflufenzopyr, quinclorac, and triclopyr. Greenhouse treatments were separated into 2 studies. The first study examined the effect of diflufenzopyr timing (0.22 kg-ai/ha). Either no diflufenzopyr was applied, or it was applied either 3 days before, tank-mixed with, or 3 days after glyphosate or imazapyr treatments. Glyphosate rates included 0.0, 0.43, 0.84, and 1.68 kg-ai/ha, while imazapyr rates included 0.0, 0.14, 0.28, and 0.56 kg-ai/ha. The second study examined PGR herbicides (2,4-D 1.12 kg-ai/ha, dicamba 0.56 kg-ai/ha, triclopyr 0.56 kg-ai/ha, and quinclorac 1.40 kg-ai/ha) tank mixed with either glyphosate or imazapyr with the previously mentioned rates. The field studies examined whether shoot stimulation from PGR herbicides (2,4-D 1.12 kg-ai/ha, dicamba 0.56 kg-ai/ha, diflufenzopyr 0.28 kg-ai/ha, triclopyr 0.42 kg-ai/ha, and quinclorac 1.40 kg-ai/ha) would result in better glyphosate or imazapyr efficacy (3.36 and 0.84 kg-ai/ha, respectively). Torpedograss treatments were all tank-mixed and applied the same day, while glyphosate or imazapyr treatments for cogongrass were applied once, on the same day (0 month) as PGR herbicides or 1, 2, or 3 months after the initial PGR herbicide application. 86

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Results from these experiments indicate that PGR herbicides provide varied levels of control when used with glyphosate or imazapyr. In the greenhouse, consistent cogongrass control came from imazapyr tank-mixed with diflufenzopyr or 2,4-D (> 80% control after 8 weeks with 0.56 kg-ai/ha of imazapyr). Torpedograss greenhouse results indicated no consistent trend in control with and without the inclusion of PGR herbicides. In the field, cogongrass was best controlled when imazapyr was applied with any PGR herbicide, for any tested intervals after PGR herbicide application, approximately 85% or greater. When glyphosate was applied 2 or 3 months after PGR herbicides, greater than 80% control was observed after 6 and 9 months. Most PGR herbicide treatments with torpedograss had no effect on glyphosate or imazapyr efficacy. It appears that cogongrass control can be improved if treated with PGR herbicides. Thus, we can conclude that we support our hypothesis for cogongrass. However, the advantage of adding/combining PGR herbicides to glyphosate or imazapyr was not observed for torpedograss. 87

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LIST OF REFERENCES Akobundu, I. O., U. E. Udensi, and D. Chikoye. 2000. Velvetbean (Mucuna spp.) suppresses speargrass (Imperata cylindrica (L.) Raeuschel) and increases maize yield. International Journal of Pest Management 46:103-108. Anderson, W. P. 1996. Weed Science: Principles and Applications, 3rd edition. St. Paul, MN: West Publishing Co. 388 p. Anonymous. 2006. BASF, The chemical corporation, Research Triangle Park, NC. Specimen label for Drive 75DF, EPA reg. no. # 7969-130. 9 p. Ayeni, A. O., 1985. Observations on the vegetative growth pattern of speargrass (Imperata cylindrica (L.) Beauv.). Agriculture, Ecosystems and Environment 13: 301-307 Ayeni, A. O., and W. B. Duke. 1985. The influence of rhizome features on subsequent regenerative capacity in speargrass (Imperata cylindrica (L.) Beauv.). Agriculture, Ecosystems and Environment 13:309-317. Bacon, P. 1986. AC 252925: A promising new compound for the control sheet alang-alang (Imperata cylindrica (L.) Beauv.). In: J.V. Pancho, S. Sasroutomo, and S. Tjitrosemito, eds. Proceedings from Weed Science Symposium, BIOTROP Special Publication No. 24 Bogor, Indones. pp. 325-339. Bahieldin, A., W. E. Dyer, and R. Qu. 2000. Concentration effect of dicamba on shoot regeneration in wheat. Plant Breeding 119(5):437-439. Baird, D. D., G. E. Baker, H. F. Brown, and V. M. Urrutia. 1983. Aquatic weed control with glyphosate in South Florida. In: Proceedings of Southern Weed Science Society 36:430-435. Barnett, J. W., J. D. Byrd, and D. B. Mask. 2001. Evaluation of 23 herbicides for control of cogongrass (Imperata cylindrica). In: Proceedings of Southern Weed Science Society 64:63. Basra, A. S. 2000. Plant Growth Regulators in Agriculture and Horticulture: Their role and commercial uses. Binghamton, NY: Food Products Press, an imprint of the Hawthorne press. 264 p. Bodle, M., and C. Hanlon. 2001. Damn the torpedograss! Wildland Weeds 4(4):9-12. Bovey, R. W., and S. G. Whisenat. 1992. Honey Mesquite (Prosopis glandulosa) control by synergistic action of cloptralid:triclopyr mixture. Weed Science 40(4):563-567. Brecke, B. J., and J. B. Unruh. 2001. Torpedograss management with quinclorac. Golf Course Management. pp. 61-64. 88

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Burke, M. J., and J. P. Grime. 1996. An experimental study of plant community invasibility. Ecology 77:776-790. Busey, P. 2003. Reduction of torpedograss (Panicum repens) canopy and rhizomes by quinclorac split applications. Weed Technology 17:190-194. Chandramohan, S., R. Charudattan, J. Devalerio, and C. Hanlon. 2003. Field trials of a bioherbicide system for integrated management of torpedograss. In: Proceedings of Invasive Plants in Natural and Managed System. Cline, M. 1994. The role of hormones in apical dominance: New approaches to an old problem in plant development. Physiologia Plantarum 90:230-237. Cline, M. G. 1997. Concepts and terminology of apical dominance. American Journal of Botany 84(8):1064-1069. Coile, N. C., and D. G. Shilling. 1993. Cogongrass, Imperata cylindrica (L.) Beauv.: A good grass gone bad! Florida Department of Agriculture and Consumer Services. Bot. Cir. No. 28. Conway Duever, L., 2003. Imperata cylindrica accessed on the Floridata website, Tallahasee, FL at HThttp://www.floridata.com/ref/I/impe_cyl.cfmTH (accessed December 14, 2006). Deregibus, J. L, M. J. Trlica, and D. A. Jameson. 1982. Organic reserves in herbage plants: Their relationship to grassland management. CRC Handbook of Agricultural Productivity. Vol. 1. Plant Productivity. M. Recheigl, Jr., ed. Boca Raton, FL: CRC Press. pp. 315-344. Dickens, R. 1974. Cogongrass in Alabama after sixty years. Weed Science 22:177-179. Dickens, R., and G. A. Buchanan. 1975. Control of cogongrass with herbicides. Weed Science 23:194-197. Dozier, H., J. F. Gaffney, S. K. McDonald, E. R. R. L. Johnson, and D.G. Shilling. 1998. Cogongrass in the United States: History, ecology, impacts, and management. Weed Technology 12:737-743. El-Midany, A. A. 2004. Separating dolomite from Phosphate rock by reactive floatation: Fundamentals and application. Ph.D. dissertation. University of Florida, Gainesville, FL. 144 p. English, R. G. 1998. The regulation of axillary bud development in the rhizomes of cogongrass (Imperata cylindrica (L.) Beauv.) M.S. thesis, University of Florida, Gainesville, FL. Eussen, J. H. H. 1979. Some competition experiments with alang-alang [Imperata cylindrica (L.) Beauv.] in replacement series. Oecologia 40:351-356. 89

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BIOGRAPHICAL SKETCH Born on September 29, 1982, Eileen is the second child of Martin and Margaret Ketterer. She grew up in Altamonte Springs, Florida, with her mother and 2 brothers, Brian and Tommy, where she attended Lyman High School. Her education continued at Bucknell University, Lewisburg, Pennsylvania, where she received her Bachelor of Science with a concentration in environmental studies. It was at Bucknell that she decided to venture into the world of weeds, completing her senior thesis on purple loosestrife. Her education culminated at the University of Florida, Gainesville, where she received a Master of Science with a concentration in agronomy, specializing in weed science. Here she studied cogongrass and torpedograss as a requirement for her masters thesis. Eileen plans to continue invasive weed eradication as well as increase public awareness on the subject. 97


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EVALUATION OF GROWTH REGULATING HERBICIDES FOR IMPROVED
MANAGEMENT OF COGONGRASS AND TORPEDOGRASS




















By

EILEEN ANN KETTERER


A THESIS PRESENTED TO THE GRADUATE SCHOOL
OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT
OF THE REQUIREMENTS FOR THE DEGREE OF
MASTER OF SCIENCE

UNIVERSITY OF FLORIDA


2007




























2007 Eileen Ann Ketterer









ACKNOWLEDGMENTS

I thank my committee chair, Dr. Greg MacDonald, for the countless hours in which he

helped me understand my lab and field work as well as making sure that everything was

executed smoothly. I thank my committee members Dr. Jay Ferrell, Dr. Ken Boote, and Dr.

Brent Sellers for their insight and expertise on my project. Special thanks to all who helped me in

the lab and the field, including Justin Snyder, Bob Querns, Danon Moxley, Tim King, Michelle

Harmeling, Chris Mudge, Brett Bultimeyer, Jing Jing Wang, Brandon Fast, and Barton Wilder. I

thank the Agronomy Department secretaries for their patience and guidance throughout my

program. I thank my family and my fiance Jeremy Guest for their continued love and support.

Lastly, I thank the Florida Institute of Phosphate Research, the Florida Department of

Environmental Protection, the Clanton Black Scholarship Fund, and the Agronomy Department

for providing me with the opportunity to research something that I enjoy.










TABLE OF CONTENTS

page
1. eg

A C K N O W L E D G M E N T S .................................................................................... .....................3

LIST OF TABLES. ..................................................................6

A B S T R A C T ....................................................................................................................... 1 1

1 IN T R O D U C T IO N ............................................................................................................. 13

B io lo g y ................................................................................................................1 3
C o g o n g ra ss ................................................................................................................. 1 3
T o rp e d o g ra ss .............................................................................................................. 1 6
M an ag em en t ....................................................................................................... ........... 17
C o g o n g ra ss ................................................................................................................. 1 7
T o rp e d o g ra ss .................. ........................................................................................... 2 0
G row th R egulating H erbicides................................................................................... 22
R atio n ale ................... ...................2...................6.........

2 INFLUENCE OF GROWTH REGULATOR HERBICIDES ON THE EFFICACY OF
GLYPHOSATE AND IMAZAPYR ON COGONGRASS UNDER GREENHOUSE
C O N D IT IO N S ............2..7...........................................

Introdu action ................... ...................2...................7..........
M materials and M methods ............................................................................................ .......29
Diflufenzopyr Timing Study .................................................................. ......... ....... ........30
Grow th Regulator Study. .............................................................31
Statistical A analysis ...................................................3 1
R esu lts .................... .. ....... ........................................................... . 3 1
D iflufenzopyr Tim ing Study ............................................. ................ .............. 31
E x p erim ent on e ............................................................................................... .......... 3 1
E xperim ent tw o .................................................................................................33
Grow th Regulator Study. .............................................................35
E xperim ent one ................................................................35
E xperim ent tw o .................................................................................................37
D iscu ssion .......................................................................... 38

3 INFLUENCE OF GROWTH REGULATOR HERBICIDES ON THE EFFICACY OF
GLYPHOSATE AND IMAZAPYR ON TORPEDOGRASS UNDER GREENHOUSE
C O N D IT IO N S ............4..6...........................................

Introdu action ................... ...................4...................6..........
M materials and M methods ............................................................................................ .......49
D iflufenzopyr T im ing Study ...................................................................................... 49
Grow th Regulator Study. .............................................................50
Statistical A analysis ......................................................................................................50


4









R e su lts .............. ................ ... .............................................................................................. 5 1
D iflufenzopyr Tim ing Study .............. ............ ........... ..................... ............... 51
Experiment one ........... ...... .......................... 51
Experiment two ........... ...... .......................... 52
G row th R egulator Study ........................................................................ ...................53
Experim ent one .............. .............................................................................53
Experim ent tw o .............. .................................................................................54
D iscu ssion ..........................................................................55

4 EVALUATION OF GROWTH REGULATOR HERBICIDES FOR IMPROVED
CON TR OL OF CO G ON G RA SS ...........................................................................................64

Introdu action ................... ...................6...................4..........
M materials and M methods ............................................................................................ .......67
M eth o d o lo g y .............................................................................................................. 6 7
S statistical A n aly sis ..................................................................................................... 6 7
R e su lts ................... ...................6...................8..........
S p rin g E x p erim en t .................................................................................................... 6 8
Sum m er Experim ent. ................................................................70
F all E xperim ent ......................................................................................................71
D iscu ssion ..........................................................................72

5 EVALUATION OF GROWTH REGULATOR HERBICIDES FOR IMPROVED
CON TR OL OF TO RPED O GR A SS .................................................................................. 80

Introdu action ................... ...................8...................0..........
M materials and M methods ............................................................................................ ....... 82
M methodology. ...................................................................82
Statistical A analysis ......................................................................................................83
R results and D discussion ............................................................................................ .......83

6 CON CLU SION S. ...................................................................86

LIST OF REFERENCES. .................................................................... 88

B IO G R A PH IC A L SK E T C H .................................................................................................... 97









LIST OF TABLES


Table .page

2-1 Overall model variance for the visual evaluation, shoot regrowth biomass, and
rhizome biomass 8 weeks after initial treatment in the cogongrass diflufenzopyr
tim ing Experim ent 1 .......................... ...................... ... ............. ......... 40

2-2 Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
in Experim ent 1 .............................................. ........................................ 40

2-3 Cogongrass shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
in Experim ent 1 ............ .. ................................................. .......... ........ .. 40

2-4 Cogongrass rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
in Experim ent 1 ............ .. .................................................. ......... ........ .. 41

2-5 Overall model variance for the visual evaluation, shoot regrowth biomass, and
rhizome biomass 8 weeks after initial treatment in the cogongrass diflufenzopyr
timing Experiment 2 ............................................. ............ 41

2-6 Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
in E xperim ent 2 ......................................................... ................. 4 1

2-7 Cogongrass shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
fo r E x p erim en t 2 ........... .................................................... .......................... .... 4 2

2-8 Cogongrass rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
fo r E x p erim en t 2 ........... .................................................... .......................... .... 4 2

2-9 Overall model variance for the visual evaluation, shoot regrowth biomass, and
rhizome biomass 8 weeks after initial treatment in the cogongrass growth regulator
E x p erim ent 1 ...................................... ................................................... 42

2-10 Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by plant growth regulating herbicides
in Experiment 1 ...................................... ................. ................ .......... 43

2-11 Cogongrass shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by plant growth regulating herbicides
in Experiment 1 ...................................... ................. ................ .......... 43









2-12 Cogongrass rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by plant growth regulating herbicides
in Experiment 1 ...................................... ................. ................ .......... 43

2-13 Overall model variance for the visual evaluation, shoot regrowth biomass, and
rhizome biomass 8 weeks after initial treatment in the cogongrass growth regulator
E x p erim ent 2 ........................................................... ................. 44

2-14 Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influences by plant growth regulating herbicides
in E xperim ent 2 ......................................................... ................. 44

2-15 Cogongrass shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influences by plant growth regulating herbicides
in E xperim ent 2 ......................................................... ................. 44

2-16 Cogongrass rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influences by plant growth regulating herbicides
in E xperim ent 2 ......................................................... ................. 4 5

3-1 Overall model variance for the visual evaluation, shoot regrowth biomass, and
rhizome biomass 8 weeks after initial treatment in the torpedograss diflufenzopyr
timing Experiment 1 ................... .................... ..... ........... 57

3-2 Percent control of torpedograss regrowth 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
in E xperim ent 1 .................................................. ........... ....... ................ 58

3-3 Torpedograss shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
in E xperim ent 1 ................................................. .................. ......................58

3-4 Torpedograss rhizome biomass (grams/pot) 8 weeks after initial treatment by
multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3
tim ings in E xperim ent 1 ................................................................... .. .............. 58

3-5 Overall model variance for the visual evaluation, shoot regrowth biomass, and
rhizome biomass 8 weeks after initial treatment in the torpedograss diflufenzopyr
timing Experiment 2 ............................................. ............ 59

3-6 Percent control of torpedograss regrowth 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
in E xperim ent 2 ......................................................... ................. 59

3-7 Torpedograss shoot regrowth (grams/pot) 8 weeks after treatment by multiple rates
of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in
E xperim ent 2 ........................................................... ................. 59









3-8 Torpedograss rhizome biomass (grams/pot) 8 weeks after initial treatment by
multiple rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3
tim ings in E xperim ent 2........................................................................... ....................60

3-9 Overall model variance for the visual evaluation, shoot regrowth biomass, and
rhizome biomass 8 weeks after initial treatment in the torpedograss growth regulator
E x p erim ent 1 ...................................... ................................................... 60

3-10 Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in
E x p erim ent 1 ...................................... ................................................... 6 0

3-11 Torpedograss shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in
E x p erim ent 1 ...................................... ................................................... 6 1

3-12 Torpedograss rhizome biomass (grams/pot) 8 weeks after initial treatment by
multiple rates of glyphosate or imazapyr, as influenced by growth regulating
herbicides in E xperim ent 1 ..................................................................... .....................61

3-13 Overall model variance for the visual evaluation, shoot regrowth biomass, and
rhizome biomass 8 weeks after initial treatment in the torpedograss growth regulator
E x p erim ent 2 ........................................................... ................. 62

3-14 Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in
E xperim ent 2 ........................................................... ................. 62

3-15 Torpedograss shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in
E xperim ent 2 ........................................................... ................. 63

3-16 Torpedograss rhizome biomass (grams/pot) 8 weeks after initial treatment by
multiple rates of glyphosate or imazapyr, as influenced by growth regulating
herbicides in E xperim ent 2. .................................................................... .....................63

4-1 Overall model variance for the control evaluations 3, 6, and 9 months after treatment
(M AT) in the cogongrass spring field experiment. ................................... .................74

4-2 Averaged across plant growth regulating herbicides, the effect of herbicide and
month of application on cogongrass control 3 months after initial plant growth
regulating herbicide application for the spring experiment.............................................75

4-3 Averaged across herbicides, the effect of plant growth regulating herbicide and
month of application on cogongrass control 3 months after initial plant growth
regulating herbicide application for the spring experiment.............................................75









4-4 Averaged across plant growth regulating herbicides, the effect of herbicide and
month of application on cogongrass control 6 months after initial plant growth
regulating herbicide application for the spring experiment.............................................75

4-5 Averaged across month of application, the effect of herbicide and growth regulator
on cogongrass control 6 months after initial plant growth regulating herbicide
application for the spring experim ent. ................................................................... ....... 76

4-6 Averaged across herbicide, the effect of growth regulator and month of application
on cogongrass control 6 months after initial plant growth regulating herbicide
application for the spring experim ent. ................................................................... ....... 76

4-7 Averaged across plant growth regulating herbicide, the effect of growth regulator
and month of application on cogongrass control 9 months after initial plant growth
regulating herbicide application for the spring experiment.............................................76

4-8 Averaged across month of application, the effect of growth regulator and herbicide
on cogongrass control 9 months after initial plant growth regulating herbicide
application for the spring experim ent. ................................................................... ....... 76

4-9 Averaged across herbicides, the effect of growth regulator and month of application
on cogongrass control 9 months after initial plant growth regulating herbicide
application for the spring experim ent. .................................................................... ...... 77

4-10 Overall model variance for the control evaluations 3 and 6 months after treatment
(MAT) in the cogongrass summer field experiment ....................................................77

4-11 Effect of growth regulator, averaged across herbicide and month of glyphosate or
imazapyr application, on cogongrass control 3 months after initial plant growth
regulating herbicide application for the summer experiment. ................. ............. .....77

4-12 Effect of month of application, averaged across herbicide and plant growth
regulating herbicides, on cogongrass control 3 months after initial plant growth
regulating herbicide application for the summer experiment. ................. ............. .....78

4-13 Averaged across plant growth regulating herbicides, the effect of herbicide and
month of application on cogongrass control 6 months after initial plant growth
regulating herbicide application for the summer experiment. ................. ............. .....78

4-14 Effect of growth regulator, averaged across herbicide and month of glyphosate or
imazapyr application, on cogongrass control 6 months after initial plant growth
regulating herbicide application for the summer experiment. ................. ............. .....78

4-15 Overall model variance for the control evaluation 3 months after treatment (MAT) in
the cogongrass fall field experiment. ...................... ................................... 78









4-16 Effect of growth regulator, averaged across herbicide and month of glyphosate or
imazapyr application, on cogongrass control 3 months after initial plant growth
regulating herbicide application for the fall experiment.............................................. ......79

4-17 Effect of month of application, averaged across herbicide and plant growth
regulating herbicide, on cogongrass control 3 months after initial plant growth
regulating herbicide application for the fall experiment.............................................. ......79

5-1 Overall model variance for the control evaluations 3 and 6 months after treatment
(M AT) in the torpedograss field experiment. ............. ............................... ............... 84

5-2 Influence of plant growth regulating herbicides applied with glyphosate and
imazapyr for control of torpedograss at 3, 6, and 9 months after treatment (MAT) ........85









Abstract of Thesis Presented to the Graduate School
of the University of Florida in Partial Fulfillment of the
Requirements for the Degree of Master of Science

EVALUATION OF GROWTH REGULATING HERBICIDES FOR IMPROVED
MANAGEMENT OF COGONGRASS AND TORPEDOGRASS

By

Eileen Ann Ketterer

May 2007

Chair: Gregory E. MacDonald
Major: Agronomy

Cogongrass [Imperata cylindrica (L.) Beauv.] and torpedograss (Panicum repens L.) are

invasive perennial grasses in Florida that cannot effectively be controlled to the point of

complete eradication without intense and often unfeasible means. The biggest hurdle in

developing a long-term management strategy for cogongrass and torpedograss is rhizome

control. Large rhizome to foliage ratio allows the plants to store photosynthates in the rhizomes.

Cogongrass rhizomes exhibit a form of apical dominance which suppresses the growth of shoots

from subapical nodes. Torpedograss, though lacking apical dominance, is primarily found in

seasonally wet or submerged aquatic settings. Herbicide efficacy on torpedograss usually

correlates with the proportion of emergent stems to the amount of herbicide interception at a

given rate. It is hypothesized that disruption of normal auxin levels in torpedograss and

cogongrass would encourage new secondary shoot production. We sought to achieve abnormal

auxin levels using plant growth regulating (PGR) herbicides and follow this with different rates

and application timings of glyphosate or imazapyr to improve efficacy.

Both greenhouse and field studies were conducted using glyphosate and imazapyr

combined in various treatments with the PGR herbicides 2,4-D, dicamba, diflufenzopyr,

quinclorac, and triclopyr. Greenhouse treatments were separated into 2 studies. The first study









examined the effect of diflufenzopyr timing (0.22 kg-ai/ha). Either no diflufenzopyr was applied,

or it was applied either 3 days before, tank-mixed with, or 3 days after glyphosate or imazapyr

treatments. Glyphosate rates included 0.0, 0.43, 0.84, and 1.68 kg-ai/ha, while imazapyr rates

included 0.0, 0.14, 0.28, and 0.56 kg-ai/ha. The second study examined PGR herbicides (2,4-D

1.12 kg-ai/ha, dicamba 0.56 kg-ai/ha, triclopyr 0.56 kg-ai/ha, and quinclorac 1.40 kg-ai/ha) tank

mixed with either glyphosate or imazapyr with the same rates as the diflufenzopyr study. The

field studies examined whether shoot stimulation from PGR herbicides (2,4-D 1.12 kg-ai/ha,

dicamba 0.56 kg-ai/ha, diflufenzopyr 0.28 kg-ai/ha, triclopyr 0.42 kg-ai/ha, and quinclorac 1.40

kg-ai/ha) would result in better glyphosate or imazapyr efficacy (3.36 and 0.84 kg-ai/ha,

respectively). Torpedograss treatments were all tank-mixed and applied the same day, while

glyphosate or imazapyr treatments for cogongrass were applied once, on the same day (0 month)

or 1, 2, or 3 months after the initial PGR herbicide application.

Results from these experiments indicate that PGR herbicides provide varied levels of

control when used with glyphosate or imazapyr. In the greenhouse, consistent cogongrass control

came from imazapyr tank-mixed with diflufenzopyr or 2,4-D (> 80% control, after 8 weeks with

0.56 kg-ai/ha of imazapyr). Torpedograss greenhouse results indicated no consistent trend in

control. In the field, cogongrass was best controlled when imazapyr was applied with any PGR

herbicide, at any of the tested intervals, providing approximately 85% control or greater. When

glyphosate was applied to cogongrass 2 or 3 months after PGR herbicides, > 80% control was

observed at 6 and 9 months. Most PGR herbicides had no effect on glyphosate or imazapyr

efficacy for torpedograss. Overall, it appears that cogongrass control can be improved if treated

with PGR herbicides, while torpedograss requires more research.









CHAPTER 1
INTRODUCTION

Cogongrass [Imperata cylindrica (L.) Beauv.] and torpedograss (Panicum repens L.) are

invasive perennial grasses (Dickens 1974, Holm et al. 1977, Wilcut et al. 1988b). Both of these

plants appear on multiple state noxious weed lists, with cogongrass also appearing on the federal

list (USDA 2005a, 2005b). While there is abundant literature on the control of cogongrass

(MacDonald 2004) and limited information on torpedograss (Sartain 2003), neither plant can be

effectively managed to the point of complete eradication without great and often unfeasible

means (Willard et al. 1997, Willard et al. 1998, Smith et al. 1999).

Biology

Cogongrass

Cogongrass is a cosmopolitan species that has been reported on every continent except

Antarctica (Coile and Shilling 1993), and currently infests over 500 million ha worldwide

(Dickens 1974, Holm et al. 1977, Flavey 1981). At least seventy-three countries report problems

with cogongrass in agricultural fields, pastures, and roadside settings (Holm et al. 1977). It is

also problematic in natural areas where it displaces native vegetation (Shilling 1996).

Introduction of cogongrass into the United States occurred around 1911 in Mobile,

Alabama, from packing material shipped from Japan (Tabor 1949). Cogongrass was also

intentionally introduced from the Philippines as a potential forage at McNeil Mississippi

Agricultural Station (Hubbard et al. 1944, Tabor 1949, Dickens and Buchanan 1975).

Cogongrass tends to invade disturbed areas with high sunlight, such as reclaimed mines,

pine plantations, pastures, rangelands, and natural areas (Willard et al. 1990, Coile and Shilling

1993, Shilling 1996). Canopy closure and shade appear to deter cogongrass establishment

(Soerjani 1970). Although not considered a shade species, studies have shown that cogongrass









adapts to shade via increases in leaf area, leaf weight ratio, and leaf area ratio (Patterson et al.

1980). Several light compensation studies also showed that cogongrass has a low compensation

point in relation to most plants (32 to 35 i mol m-2 s-1) indicating survival even in highly

competitive and light limiting environments (Gaffney 1996, Jose et al. 2002).

Cogongrass exhibits many features that allow it to be highly competitive. The silica bodies

on the edge of mature leaves deter herbivory (Coile and Shilling 1993). This, coupled with poor

quality, makes it unpalatable and unsuitable as a forage crop (Coile and Shilling 1993). The

pyrogenic nature of cogongrass also contributes to its success as a weed (Patterson et al. 1980).

Dead cogongrass leaves do not detach and decompose, but remain on the plant and become

highly flammable when desiccated (Coile and Shilling 1993). Although many native grasses in

the southeastern United States are adapted to fire ecology, the fires that occur in cogongrass

communities are hotter and more intense, resulting in the displacement of native vegetation

(Lippincott 2000, Rossiter et al. 2003). Studies have also shown that cogongrass exudes

allelopathic compounds from both foliage and roots (Koger and Bryson 2003) which deter the

vegetative growth of specific plants near existing or recently removed stands of cogongrass

(Inderjit and Dakshini 1991, Hussain et al. 1992, Johnson et al. 1997, Koger and Bryson 2003).

This allelopathy has also been shown to suppress germination and seedling growth of certain

crops (Inderjit and Dakshini 1991, Koger and Bryson 2003).

This plant has the ability to invade, not only on disturbed areas, but also in vegetatively

intact communities via seeds (King and Grace 2000). Cogongrass produces over 3000 seeds per

plant (Holm et al. 1977) of which 80 to 90% are viable (Shilling et al. 1997). However, optimum

seed germination occurs immediately after seed set and rapidly declines after 3 months with

almost complete loss of viability after one year (Shilling et al. 1997). Viable cogongrass seeds









are reported to be only produced through out-crossing (Gabel 1982, McDonald et al. 1996).

There are conflicting reports regarding cogongrass seed dispersal in Florida. Willard and Shilling

(1990) suggested that rhizomes were solely responsible for cogongrass spread. This theory was

supported by McDonald et al. (1996) who did not detect out-crossing in Florida. However,

Shilling et al. (1997) did collect viable seeds, suggesting that out-crossing occurs or a different

population has developed in this area since the results from the 1990 study by Willard et al.

(1990).

Cogongrass rhizomes begin to form soon after seed germination or rhizome sprouting

(Ayeni 1985). Eussen (1979) reported eleven weeks after initial rhizome growth, the rhizome

mass may occupy an area as large as 4m2. In a mature stand, cogongrass can develop as many as

350 shoots from its rhizome mass in a 6-week period (Eussen 1979). A mature and densely

populated stand of cogongrass can have rhizomes weighing as much as 40 tons fresh weight per

hectare (Terry et al. 1997, English 1998).

Rhizomes comprise greater than 60% of total biomass (Sajise 1976) and Terry et al. (1997)

suggested that cogongrass may even sacrifice leaf production to maintain this high ratio (Sajise

1972, Sajise 1976). As it grows, the rhizomes branch out in many directions, forming a dense

rhizomatous mat. This mat excludes vegetative roots or rhizomes of other species from becoming

established within a cogongrass stand (Dozier et al. 1998). Cogongrass rhizomes are very

resistant to high temperatures and fire has been hypothesized to stimulate dormant rhizome buds,

promoting larger, denser cogongrass stands (Coile and Shilling 1993).

Rhizomes have an incredible regeneration capacity and this capacity is positively

correlated with increased weight, height, age, length, thickness of rhizomes, and visible buds

(Ayeni 1985). Regeneration cannot occur with newly formed rhizomes as they lack roots and









therefore the ability to take up nutrients (Ayeni 1985, Ayeni and Duke 1985). Success of

rhizome regeneration also depends upon depth of burial (Lee 1977, Wilcut et al. 1988a), the

location of the rhizome segment on the original rhizome, and the proximity to the apical buds

(Holm et al. 1977, Gaffney 1996, Wilcut et al. 1988a, English 1998).

Torpedograss

Torpedograss is an old world Eurasian plant (Holm et al. 1977). Although the exact reason

for introduction is unknown, it is speculated that torpedograss either came to the Southeastern

United States via ship ballasts or was introduced as a potential wetland forage (Tabor 1952). In

the United States, torpedograss is found from Florida to Texas (Wilcut et al. 1988a, McCarty et

al. 1993). This plant is most frequently found near or in aquatic sites (Holm et al. 1977) and

Florida Department of Environmental Protection ranks torpedograss as the 2nd most abundant

plant in Florida lakes (Schardt 1992, Schardt personal communication, February 2007). It can

also be found on terrestrial areas such as golf courses and roadsides (Brecke and Unruh 2001).

The presence of torpedograss is problematic in Florida because it interrupts flood control,

irrigation and turf production (Shilling and Haller 1989, McCarty et al.1993).

While torpedograss produces seeds, reports suggest these seeds may be non-viable and the

primary means of reproduction is through rhizomes (Wilcut et al. 1988a, Ferriter et al. 2006).

However, viability and spread from seed has been reported in Portugal (Peng 1984).

Similar to cogongrass, torpedograss rhizomes comprise approximately 70 to 90% of the

total biomass (Smith et al. 1999). This plant also has a very high rhizome regeneration rate (92 to

96% of rhizome buds at 20 to 35C) from small segments (Hossain et al. 2001). Torpedograss

produces new buds along the entire length of the rhizome contributing to the dense rhizome mass

(Wilcut et al. 1988a).









Management

Complete control of cogongrass and torpedograss requires total removal of all viable tillers

and rhizomes (Tanner et al. 1992, Willard et al. 1997, Smith et al. 1999). There have been

numerous studies to identify best management practices for the control of these plants, but none

have yielded 100% control longer than 24 months within time constraints and budgets (Willard

et al. 1997, Willard et al. 1998, Smith et al. 1999). Another issue in natural areas is that lands are

set aside for conservation of the native plant community (Langeland and Stocker 2001). There is

a need for management in these natural areas that will not damage desirable, non-target species

(Halpin 1997, Langeland and Stocker 2001). Since both cogongrass and torpedograss occur in

natural areas, management strategies employing mechanical or cultural methods may not be

practical.

Cogongrass

Biological control for cogongrass has been disappointing with very few, if any, organisms

providing appreciable control (Soerjani 1970, Coile and Shilling 1993). Recent studies indicate a

host of organisms are found on this plant, including fungi, insects, nematodes, mites and one

parasitic plant (Minno and Minno 1999, Minno and Minno 2000). While there is still a chance

that one or more of these organisms could be used as a control, there is no conclusive evidence

that would suggest any successful biological control agents. Biological control studies are

currently being conducted in conjunction with other control methods (Yandoc et al. 2004,

Yandoc et al. 2005).

There have been a number of studies that utilize cover crops as a cultural technique to

control cogongrass (Menz and Grist 1996, Otsamo et al. 1997, Akobundu et al. 2000, Versteeg

and Koudokpon 1990). This approach suggests that landholders consider long-term management

involving the use of other crops to crowd out cogongrass (MacDonald 2004). Crops can include









legumes such as velvetbean (Mucunapruriens var. utilis) (Versteeg and Koudokpon 1990,

Akobundu et al. 2000), and rubber trees (Hevea brasiliensis) (Menz and Grist 1996), as well as

other species. These crops can slow and reduce cogongrass growth in as few as 2 to 5 years

(Akobundu et al. 2000). Studies have also included the use of other exotic tree species that are

fast growing and quick to shade out and suppress cogongrass (Otsamo et al. 1997). Others have

also shown cogongrass seedlings to be suppressed by greater than 75% with bahiagrass cover

(Willard and Shilling 1990, Shilling et al. 1997). While these techniques may be beneficial in

agricultural settings, these methods cannot be utilized in natural areas where the preservation of

desirable species is a priority in addition to controlling cogongrass (Langeland and Stocker

2001).

Mechanical approaches such as discing, mowing, and fire to control cogongrass have had

mixed results (Wilcut et al. 1988a, Coile and Shilling 1993, McCarty et al. 1993, Lippincott

1997). Studies have shown that cogongrass cannot survive in heavily cultivated areas (Coile and

Shilling 1993). Deep tilling during the dry season exhausts the food supply by drying out

rhizomes (Soerjani 1970, Johnson et al. 1997), and burying the rhizomes to a depth where

growth of new shoots is less likely, > 8cm (Ivens 1980, Wilcut et al. 1988a). Deep and repeated

tillage breaks apical dominance, promoting shoot growth, thus increasing the amount of

herbicide that is absorbed in chemical applications (Willard et al. 1996). However, frequency of

tilling is an important factor in controlling cogongrass, as Johnson et al. (1999) reported that

infrequent cogongrass discing may be ineffective and might promote the species. Mechanical

control is not always an option for control in natural areas as the soil disturbance and heavy

equipment may provide more damage than benefit (Langeland and Stocker 2001).









The use of fire has been considered and implemented for cogongrass control, but thus far,

it only seems to promote cogongrass (Lippincott 1997). Fire temperatures, duration, and

intensities are well below what is needed to desiccate cogongrass rhizomes (Holm et al. 1977,

Soerjani 1970). Unless cogongrass rhizomes can be directly burned after mechanical control has

been utilized, this is not an effective control option.

A number of chemical control studies have been performed on cogongrass (Dickens and

Buchanan 1975, Baird et al. 1983, Bacon 1986, Lee 1986, Tanner et al.1992). Herbicide

applications to cogongrass are difficult due to the level of dead leaves preventing total herbicide

coverage (Coile and Shilling 1993). Studies involving graminicides (grass specific herbicides)

have shown that these chemicals have little effect on cogongrass (Mask et al. 2000). Those

herbicides having the best results include glyphosate N-(phosphonomethyl)glycine, imazapyr 2-

[4,5-dihydro-4-methyl-4-(1-methylethyl)-5-oxo-1-H-imidazol-2-yl]-3-pyridinecarboxylic acid,

and dalapon (2,2-Dichloropropionic acid, no longer registered) (Willard et al. 1997).

Glyphosate produces rapid cogongrass defoliation (Townsend and Butler 1990) with no

soil residual activity (WSSA 2002). Young cogongrass leaves, possibly due to less developed

cuticles, are most susceptible to glyphosate treatment (Lee 1986). A thicker cuticle would help

prevent the entry of harmful substances (e.g., too much sunlight or herbicides) (Wanamarta and

Penner 1989). Imazapyr is slower acting, but provides better long term control due to residual

soil activity (Johnson et al. 1997, Willard et al. 1997).

There have been several reports that herbicide applications in the fall provide increased

control with glyphosate or imazapyr (Gaffney 1996, Johnson et al. 1999). Johnson et al. (1997)

reported imazapyr (0.84 kg-ai/ha) and glyphosate (2.24 kg-ai/ha) provided 70 to 80% control up

to 1 year after treatment when applied in the fall. Gaffney (1996) also indicated > 20% more









control was achieved 1 year after treatment with the same herbicides and rates in a fall

application versus a spring or summer application.

Torpedograss

Very little biological control research has been done on torpedograss due to the reluctance

to use this method on grasses in general (Bodle and Hanlon 2001). Chandramohan et al. (2003)

indicated that three native fungi (Drechslera gigantea, Exserohilum longirostratum, and E.

rostratum) may manage torpedograss for 7 to 9 months. The option of biological control is

expanding but more research is needed in this area.

Mechanical techniques do not have the same effect on torpedograss as with cogongrass.

Instead, torpedograss is actually promoted by cultivation, as any fragmentation of the rhizomes

can result in a large amount of new plants in a short amount of time after a 4 week lag phase

(Holm et al. 1977, Wilcut et al. 1988a, Sutton 1996,). Even simple maintenance techniques such

as core aeration have been shown to increase torpedograss density in turf (McCarty et al. 1993).

The invasion of torpedograss is due, in part, to a lack of strong apical dominance in rhizomes as

well as high rhizome regeneration rate (similar to cogongrass) and an increased ability to store

water and nutrients in times of stress (Wilcut et al. 1988a).

As with cogongrass, torpedograss is not adversely affected by burning alone (Hanlon and

Langeland 2000). However, it appears that the best form of torpedograss control occurs when

herbicide application follows a bur. In a study by Hanlon and Langeland (2000) there was little

long term control of torpedograss if it was not burned prior to herbicide treatment. When

evaluated 42 weeks after treatment, imazapyr applied 6 weeks after a burn provided 65 to 85%

control, compared to < 20% when applied to non-burned plants.

There have been several herbicide control studies on torpedograss but the herbicides

glyphosate and imazapyr provide the most acceptable control (Baird et al. 1983, Shilling and









Haller 1989, Willard et al. 1998, Smith et al. 1999, Hanlon and Langeland 2000). Both

herbicides are broad-spectrum herbicides. However, glyphosate has little to no soil residual

activity, whereas the residual activity of imazapyr is high due to its long soil half-life, 25 to 142

days (WSSA 2002).

Limited control from glyphosate is often attributed to the aquatic habitat of torpedograss.

When the plant is treated under such conditions, the herbicide only reaches the emergent portion

(Smith et al. 1999). Studies show that this portion of the plant usually dies but regrowth from

rhizomes and submerged stems segments often occurred within a few months (Baird et al. 1983).

Smith et al. (1999) concluded that high water levels inhibit foliar interception of glyphosate and

control correlated with foliar exposure to water level ratio. To achieve > 90% control (5 weeks

after initial treatment), a glyphosate application rate of 2.24 kg-ai/ha was needed to be

intercepted by at least 40% of the foliage. Lower rates correlated with a higher percentage of

foliage cover to achieve similar results (Smith et al. 1999).

Imazapyr applications on torpedograss have produced similar problems with submergence

and in turn, less control (Hanlon and Langeland 2000). Inconsistencies in data presented by

Hanlon and Langeland (2000) lead the authors to speculate that fluctuating water depth at

different experimental sites could have influenced results. While all experiments began in

approximately 0.8 meters of water, by the end of the experiment, one study site was considered

dry while the remaining sites were flooded. Greater than 95% control was observed at the dry

site with < 25% control at the flooded sites. The authors also speculated that thatch levels may

have contributed to inconsistent control. The amount of torpedograss tissue exposed to the

herbicide may be reduced as thatch increased (Hanlon and Langeland 2000).









Growth Regulating Herbicides

As previously mentioned, both cogongrass and torpedograss have a high rhizome to shoot

ratio, contributing to their success (Sajise 1976, Smith et al. 1999). Having a high rhizome:shoot

ratio allows for the build up of carbohydrate reserves. These reserves have long been thought to

mobilize when photosynthetic material is reduced, such as defoliation through herbicide

application or other means (White 1973, Deregibus et al. 1982). However, other studies have

shown that plant growth may be the result of activating molecules as well as carbohydrate

reserves and may involve bud activation (Watson and Casper 1984, Richards and Caldwell

1985). When buds are suppressed, carbohydrate reserves accumulate (White 1973).

Bud suppression is mostly due to plant hormones such as auxins or cytokinins (Cline

1997). Cytokinins work to stimulate cell division (Taiz and Zeiger 2006). When lateral rhizome

buds are formed cytokinins are promoted at the site (Cline 1997). Once the rhizomes form the

apexes, then auxins are released (Cline 1997). These auxins will suppress buds growing below

the apex (Cline 1997, Taiz and Zeiger 2006). The level of apical dominance exhibited in a plant

depends upon the level of auxins present in the apex (Cline 1997). The ratio of auxins to

cytokinins determines whether rhizome production or shoot production will increase. A high

auxin:cytokinin ratio equates to more root/rhizome production, whereas a low ratio causes more

shoot production (Taiz and Zeiger 2006). In the event of a physical removal of a rhizomatous

apex, cytokinins are released and auxin decreases (Cline 1997). Subapical buds begin to grow as

the auxin:cytokinin ratio decreases (Taiz and Zeiger 2006). Once these subapical buds begin to

grow, auxins and gibberellins are then promoted again (Cline 1997). Gibberellins stimulate shoot

production (Taiz and Zeiger 2006).

Plant growth regulating herbicides (PGR herbicides) are widely used for weed control

(Sprecher and Stewart 1995, Ketchersid and Senseman 1998, Grossman et al. 2002, Lym and









Deibert 2005). Diflufenzopyr [2-(1-[([3,5-difluorophenylamino]carbonyl)-hydrazono]ethyl)-3-

pyridinecarboxylic acid], triclopyr [(3,5,6-trichloro-2-pyridinyl)oxy], picloram (4-amino-3,5,6-

trichloro-2-pyridinecarboxylic acid), clorpyralid (3,6-dichloro-pyridine carboxylic acid),

quinclorac (3,7-Dichloro-8-quinolinecarboxylic acid), dicamba (3,6-dichloro-2-methoxybenzoic

acid), and 2,4-D [(2,4-dichlorophenoxy) acetic acid] are commonly used PGR herbicides

(Anderson 1996, Ketchersid and Senseman 1998, Grossman et al. 2002). Herbicides in this

classification interfere with growth hormone functions and have similar modes of action and

selectivity (Anderson 1996). While the true mode of action of some of these herbicides is

unknown, it is speculated that some of these PGR herbicides have auxin-like properties which

mimic auxins in an unregulated fashion (e.g., 2,4-D, dicamba, diflufenzopyr, quinclorac) (WSSA

2002). Other growth regulating herbicides such as diflufenzopyr inhibit the transport of auxins

(Grossman et al. 2002, WSSA 2002). By mimicking or interfering with auxins, PGR herbicides

interfere with nucleic acid metabolism, and upset normal hormone balance, cell enlargement,

protein synthesis, and even respiration (Anderson 1996). Auxin-like compounds have been used

in agriculture and horticulture for years to promote growth for desirable species (Basra 2000).

Sugarcane (Saccharum spp. hybrids) is an example of a crop that uses auxin-like compounds to

increase regeneration rate for vegetatively propagated plants as necessitated by the high demand

for genetically uniform sugarcane products in consumer diets (Franklin et al. 2006).

Diflufenzopyr in conjunction with the herbicide dicamba has been studied as an option in

controlling broadleaf invasive plants (Grossman et al. 2002). Studies involving the invasive

broadleaf plants leafy spurge (Euphorbia esula L.) and Canada thistle (Cirsium arvense L.),

showed the combination of diflufenzopyr and dicamba provided superior control compared to

either herbicide alone (Lym and Deibert 2005).









Application timing of diflufenzopyr appears to be critical for control (Ketchersid and

Senseman 1998). The combination of diflufenzopyr and dicamba proved more phytotoxic to

other broadleaves such as field bindweed (Convovulus arvense L.) and velvetleaf (Abutilon

theophrasti Medic.) when diflufenzopyr was applied 3 days before the herbicide compared to

diflufenzopyr in conjunction with or after application (Ketchersid and Senseman 1998).

Broadleaf plants can be controlled efficiently with diflufenzopyr (Lym and Deibert 2005), but

little is known about diflufenzopyr in grasses, specifically invasive perennial grasses.

Triclopyr is primarily used to control woody and broadleaf species (WSSA 2002). There is

either limited information or lack of positive results for the use of triclopyr in invasive grasses

(WSSA 2002). In aquatic studies, this herbicide has high selectivity for certain invasive species

while causing little damage to native plants, such as Eurasian watermilfoil (Myriophyllum

spicatum L.) (Sprecher and Stewart 1995).

2,4-D and dicamba are both speculated to be auxin mimics. These two herbicides along

with triclopyr increase the evolution of ethylene which produces uncontrolled growth known as

epinasty (WSSA 2002). 2,4-D is a long standing herbicide which has primarily been used in

broad situations from agriculture and pastures, to aquatics (WSSA 2002). While this herbicide

has been reported to have little or no activity on grasses, it does control a wide range of broadleaf

weeds (WSSA 2002). Dicamba can be applied as a PRE or POST emergence application. It is

used on pastures, turf, and some row crops (WSSA 2002). Unlike 2,4-D this herbicide does have

some activity on grasses as well as many broadleaf weeds such as Canada thistle (WSSA 2002).

While there are limited data on the effects of quinclorac on cogongrass, torpedograss is

moderately susceptible to this herbicide (Anonymous 2006). Quinclorac is labeled for

torpedograss control in bermudagrass (Cynodon dactylon) (Anonymous 2006). However,









multiple applications are necessary to achieve acceptable control. McCarty et al. (1993)

concluded that multiple quinclorac applications at 2.2 kg-ai/ha followed by 1.1 kg-ai/ha 3 and 6

weeks after initial treatment (WAT) could control torpedograss (85 to 90% control) for 7 to 10

WAT. Busey (2003) found 4 applications at 0.42 kg-ai/ha a year for 2 years reduced

torpedograss dry weight 80%.

While absorption and translocation of quinclorac occur in both the foliage and the roots, it

is more often absorbed and translocated through the roots of torpedograss (Williams et al. 2004).

A study by Williams et al. (2004) indicated that at 4 WAT the fresh weight foliage of

torpedograss was reduced 39% regardless of rate (0.56, 0.78, 1.01, and 1.23 kg-ai/ha) when

quinclorac was applied directly to the soil, compared to soil and foliar application and foliar

application alone (36 and 21% respectively). However, at 7 WAT, foliage was reduced 74% with

the foliar and soil combined application of quinclorac compared to foliar and soil applications

alone (25 and 40% reduction, respectively). At 10 WAT, foliage reduction was highest with the

foliar application alone (26%) and soil application alone had the least foliage reduction (2%).

Williams et al. (2004) speculated that soil-applied quinclorac may have leached out of the

rooting zone indicating that there could be adverse effects of quinclorac if applied to

torpedograss in a submersed area (Williams et al. 2004).

Although seeds are a concern with cogongrass, the biggest hurdle in developing a viable

management strategy for cogongrass and torpedograss is control of rhizomes. While apical

dominance is weak in torpedograss rhizomes, cogongrass rhizomes exhibit a strong form of

apical dominance which suppresses the growth of shoots from subapical nodes (Wilcut et al.

1988a, Cline 1994, Gaffney and Shilling 1995). Gaffney (1996) reported that cogongrass

rhizomes with apices removed produced 31% more shoots than rhizomes with intact apices.









Therefore, disruption of normal auxin levels in rhizome grasses could encourage new shoot

production of otherwise dormant buds (Cline 1994, English 1998). This generally occurs with

physical injury, but it has been hypothesized that plant growth regulator herbicides could cause

this effect as well. As for torpedograss, rhizome manipulation may result in increased emergent

shoots. This too may be achieved using PGR herbicides. Since cogongrass and torpedograss

occur in areas that preclude mechanical disturbance, the use of growth regulating herbicides in

conjunction with current control methods warrants research.

Rationale

Herbicide treatments often do not provide complete control of cogongrass or torpedograss,

although field observations have shown increased levels of control with different combinations

of growth regulating herbicides. We hypothesize that herbicides are unequally distributed among

meristematic regions in the rhizomes, perhaps because of apical dominance in cogongrass or the

aquatic habitat of torpedograss. These studies will address the hypothesis that the combination of

plant growth regulating herbicides with glyphosate or imazapyr will increase herbicide efficacy

in cogongrass and torpedograss by providing more complete distribution of herbicides. The

specific objectives follow:

* Determine the effect of diflufenzopyr application timing on the efficacy of glyphosate and
imazapyr on cogongrass and torpedograss under greenhouse conditions

* Determine the effect of growth regulating herbicides on the efficacy of glyphosate and
imazapyr on cogongrass and torpedograss under greenhouse conditions

* Determine the impact of growth regulating herbicides on the control of cogongrass and
torpedograss with glyphosate or imazapyr under field conditions









CHAPTER 2
THE INFLUENCE OF GROWTH REGULATOR HERBICIDES ON THE EFFICACY OF
GLYPHOSATE AND IMAZAPYR ON COGONGRASS UNDER GREENHOUSE
CONDITIONS

Introduction

Cogongrass [Imperata cylindrica (L.) Beauv.], an invasive perennial grass, is considered

noxious by both state and federal agencies (Dickens 1974, Holm et al. 1977, USDA 2005a,

2005b). While there is abundant literature on the control of cogongrass (MacDonald 2004), these

reports indicate that sustaining high levels of control cannot be accomplished without intense and

often unfeasible means (Willard et al. 1997). For example, landowner can expect to pay greater

than $200/ha per year for chemical control alone (Ramsey et al. 2003, as cited in Matta and

Alavalapati 2007). Even with this level of expense, only 2 to 3 years of 40 to 60% control, at

most, will be observed (Willard et al. 1996, Willard et al. 1997).

A number of herbicidal studies have been performed on cogongrass (Dickens and

Buchanan 1975, Baird et al. 1983, Bacon 1986, Lee 1986, Tanner et al. 1992, Barnett et al.

2001). Those herbicides having the best results are limited to glyphosate N-(phosphonomethyl)

glycine and imazapyr 2-[4,5-dihydro-4-methyl-4-(1 -methylethyl)-5-oxo-1 -H-imidazol-2-yl]-3-

pyridinecarboxylic acid (Willard et al. 1997). Willard et al. (1996) reported that glyphosate and

imazapyr provide roughly 40 to 60% control on cogongrass 2 years after treatment. Glyphosate

produces almost immediate cogongrass defoliation, with no soil residual activity (Townsend and

Butler 1990). Imazapyr is slower acting, but provides better long term control due to residual soil

activity (Johnson et al. 1997, Willard et al. 1997). Applications of 3.4 kg-ai/ha of glyphosate and

0.8 kg-ai/ha of imazapyr provided 60 and 70% control of regrowth 19 months after initial

treatment, respectively, when applied alone (Willard et al. 1997). However, when glyphosate and









imazapyr were sequentially applied, control ranged from 87 to 98% 19 months after initial

treatment regardless of application order (Willard et al. 1997).

One of the major reasons that cogongrass is such a successful invader is due to its

extensive rhizome system. Rhizomes comprise greater than 60% of the entire plant's biomass

(Sajise 1976). Eussen (1979) reported eleven weeks after initial rhizome growth, the rhizome

mass may occupy an area as large as 4m2. In a mature stand, cogongrass can develop as many as

350 shoots from its rhizome mass in a 6-week period (Eussen 1979). Rhizomes can produce as

much as 40 tons fresh weight per ha in dense stands (Terry et al. 1997, English 1998). Rhizomes

exhibit a form of apical dominance which suppresses the growth of shoots from subapical nodes

(Cline 1994).

Due to its extensive rhizome network, all viable tillers and rhizomes of cogongrass must be

controlled to prevent regrowth (Tanner et al. 1992, Willard et al. 1997). Numerous studies

involving biological, mechanical, cultural, and chemical control have indicated that the most

consistent and effective method for cogongrass control is through herbicide application.

However, the best management practices for cogongrass, regardless of method or integration of

methods have not yielded 100% long term control (> 24 months) within time constraints and

budgets for the average landowner (Willard et al. 1997).

Poor, long term herbicide control may be the result of apical dominance, possibly causing

unequal distribution of carbohydrates and, consequently, systemic herbicides in the rhizomes.

Studies on auxins suggest that these hormones play a role in apical dominance in cogongrass

(Gaffney and Shilling 1995). Gaffney (1996) reported that cogongrass rhizomes with apices

removed produced 31% more shoots than rhizomes with intact apices. Therefore, disruption of

normal auxin levels in cogongrass could encourage new shoot production of otherwise dormant









buds (Cline 1994, English 1998). This generally occurs with physical injury, but it has been

hypothesized that plant growth regulating herbicides (PGR herbicides) could cause this effect as

well. By disrupting apical dominance, systemic herbicides may be distributed more evenly and

potentially provide more complete control.

There are several herbicides that interfere with normal auxin function in plants. These

include triclopyr, 2,4-D, dicamba, quinclorac, and diflufenzopyr (WSSA 2002). It is speculated

that some of these PGR herbicides have auxin-like properties that mimic auxins in an

unregulated fashion with plants, while others block the transport of auxins (Anderson 1996,

WSSA 2002, Lym and Deibert 2005). Previous research by English (1998) studied the impact of

some growth regulating herbicides on bud break in cogongrass and found that diflufenzopyr

increased sprouting in 21% of previously dormant buds, using a 0.5 ppm concentration. Other

growth regulating herbicides such as 2,4-D resulted in < 10% bud break at 5 ppm and did not

differ from untreated plants.

Since cogongrass occurs in areas that preclude mechanical disturbance, the use of growth

regulating herbicides in conjunction with current control methods warrants research. The

application timing of diflufenzopyr and the combination of glyphosate or imazapyr with growth

regulating herbicides has never been studied on cogongrass. Thus, this study has two objectives:

1.) determine the effect of diflufenzopyr application timing on the efficacy of glyphosate and

imazapyr on cogongrass, and 2.) determine the effect of growth regulating herbicides, other than

diflufenzopyr, on the efficacy of glyphosate and imazapyr on cogongrass.

Materials and Methods

Cogongrass plants were established from rhizomes that were obtained from local

Gainesville populations. Plants were grown under greenhouse conditions with the following









environmental parameters: 12 hr day, 12 hr night, temperature 30/20C. Cogongrass was grown

in 3L pots with commercial potting soil.1 and amended with slow-release fertilizer.2.

Plants were grown for 8 to 10 weeks to ensure a dense and healthy rhizome mass.

Treatments for both studies were applied using a standard small plot sprayer with appropriate

nonionic surfactant (0.25% v/v) and a spray volume of 187L/ha. Shoot biomass was removed 4

weeks after initial treatment (WAIT) and plants were then allowed to regrow for 4 weeks. After

this time period, visual assessments (0 = no control, 100 = complete control) on shoot regrowth

were performed and shoot regrowth and root biomass were collected. Samples were placed in a

forced air oven at 70 C for 3 days and dry weights recorded.

Diflufenzopyr Timing Study

This study was a 4 (diflufenzopyr timings) by 2 (glyphosate or imazapyr) by 4 (rates)

factorial in a completely randomized design. Diflufenzopyr was selected specifically for this

study because it has been determined through research by English (1998) and Gaffney (1996) to

have caused a greater level of cogongrass bud break. Treatments for this study included

diflufenzopyr applied at a rate of 0.22 kg-ai/ha 3 days prior, in conjunction, or 3 days after the

application of glyphosate or imazapyr. Glyphosate and imazapyr rates included 0.0, 0.43, 0.84,

or 1.68 kg-ai/ha, and 0.0, 0.14, 0.28, or 0.56 kg-ai/ha, respectively. Three diflufenzopyr timings

were chosen because it was uncertain when axillary shoot growth would be stimulated. Controls

consisted of untreated plants, only surfactant treatment, and diflufenzopyr alone treatments.

Experiment one occurred from 24 October 2005 19 December 2005 and experiment two

occurred from 12 May 2006 7 July 2006.



.1 Metro mix Agricultural Lite Mix
2 Scotts Osmocote 14-14-14









Growth Regulator Study

This study was a 4 (growth regulating herbicides) by 2 (glyphosate or imazapyr) by 4

(rates) factorial in a completely randomized design. In this study, PGR herbicides were applied

to actively growing cogongrass in conjunction with glyphosate and imazapyr. The rates for

dicamba, 2,4-D, triclopyr, and quinclorac were 0.56, 1.12, 0.56, and 1.4 kg-ai/ha, respectively.

The glyphosate and imazapyr rates were the same as reported for the diflufenzopyr study.

Experiment one occurred from 7 March 2006 to 2 May 2006 and experiment two occurred from

28 April 2006 to 23 June 2006.

Statistical Analysis

The data were analyzed using proc GLM program in SAS 9.1. Models for the independent

variables (experiment, growth regulating herbicides or timing, herbicide, and rate) were

determined using the dependent variables (visual evaluations, and shoot regrowth and

rhizome/root biomass harvests). Data are reported as p-values for interaction and means with

95% confidence intervals for statistical difference. All studies were conducted twice with 4

replications.

Results

Diflufenzopyr Timing Study

Analysis of variance indicated a significant (p < 0.05) treatment by experiment interaction

therefore experiments are presented separately.

Experiment one

Visual evaluation. There was a significant (p < 0.05) three-way interaction among

diflufenzopyr timing, herbicide, and herbicide rate for the visual evaluation (Table 2-1). When

glyphosate was applied alone at 0.43 kg-ai/ha, or when diflufenzopyr was applied 3 days prior to,

or 3 days after glyphosate at this rate, < 8% control was observed (Table 2-2). However, when









glyphosate was applied tank-mixed with diflufenzopyr, nearly 50% control was observed. This

tank-mixed treatment did not differ from the previously mentioned diflufenzopyr application

occurring 3 days after glyphosate application. Glyphosate (0.84 kg-ai/ha) applied alone or with

diflufenzopyr applied 3 days after provided no observed control. Treatments tank-mixed at this

rate (0.84 kg-ai/ha) provided more control compared to glyphosate alone. Diflufenzopyr had no

effect on glyphosate at the highest rate (1.68 kg-ai/ha).

Imazapyr (0.14 kg-ai/ha) with diflufenzopyr applied 3 days before or tank-mixed provided

more cogongrass control compared to imazapyr alone (Table 2-2). Diflufenzopyr had no effect

on the 2 highest imazapyr rates (0.28 and 0.56 kg-ai/ha). The diflufenzopyr treatments did not

differ across rates, all providing > 88% control with any application timing.

Shoot regrowth. There were significant two-way interactions (p < 0.05) between all

treatment variables (timing and herbicide, herbicide and rate, and timing and rate) for shoot

regrowth in experiment 1 (Table 2-1). No glyphosate treatments reduced shoot regrowth

compared to the untreated controls (0.8 0.4 grams/pot) (Table 2-3). Diflufenzopyr, when tank-

mixed with glyphosate (0.43 kg-ai/ha), reduced regrowth compared to glyphosate alone.

However, diflufenzopyr had no effect at the highest rates (0.84 and 1.68 kg-ai/ha). Herbicide rate

had no effect for most glyphosate treatments, glyphosate (1.68 kg-ai/ha) alone or with

diflufenzopyr applied 3 days after are the exceptions. These treatments reduced shoot regrowth

compared to these same treatments at lower rates.

All imazapyr treatments reduced shoot regrowth compared to the untreated control (0.8 +

0.4 grams/pot) (Table 2-3). The addition of diflufenzopyr to the lower imazapyr rate (0.14 kg-

ai/ha) greatly reduced shoot regrowth to < 0.1 grams/pot. Diflufenzopyr had no effect when the









rate of imazapyr increased (0.28 and 0.56 kg-ai/ha). However regrowth for all treatments at these

rates did not exceed 0.1 grams/pot.

Rhizome biomass. There was a high level of variability within experiment 1, resulting in

no differences among treatments (Table 2-1). Treatments also did not differ in comparison to the

untreated controls (8.8 10.0 grams/pot) (Table 2-4).

Experiment two

Overall model variance for experiment 2 parameters, including visual evaluation, shoot

regrowth biomass and rhizome/root biomass are listed in Table 2-5.

Visual evaluation. There was a significant (p < 0.05) three-way interaction among timing,

herbicide, and herbicide rate for the visual evaluation (Table 2-5). At any rate or diflufenzopyr

timing, < 50% control was observed for glyphosate (Table 2-6). The addition of diflufenzopyr

had no effect at the lowest and highest glyphosate rates (0.43 and 1.68 kg-ai/ha). When

glyphosate (0.84 g-ai/ha) was applied alone there was almost no control. Diflufenzopyr applied 3

days before or 3 days after glyphosate provided more control compared to glyphosate alone.

Glyphosate alone at the lowest and highest rates (0.43 and 1.68 kg-ai/ha) provided more control

compared to the intermediate rate of glyphosate (0.84 kg-ai/ha).

Cogongrass control from imazapyr in experiment 2 was influenced greatly by

diflufenzopyr timing treatments (Table 2-7). Greater than 90% control was observed with

imazapyr (0.14 kg-ai/ha) when tank-mixed with diflufenzopyr. Similar levels of control were

also observed with the 2 highest imazapyr rates (0.28 and 0.56 kg-ai/ha) when tank-mixed with

diflufenzopyr. Control observed with imazapyr alone at 0.28 kg-ai/ha did not differ from the

tank-mixed treatments, but it also did not differ from treatments with diflufenzopyr applied 3

days before or 3 days after. The effect of diflufenzopyr was not observed at the highest rate (0.56

kg-ai/ha). However, all treatments at this rate provided > 50% control. Control from the lowest









and highest rates of imazapyr (0.14 and 0.56 kg-ai/ha), with diflufenzopyr applied 3 days after,

exceeded the control provided by the intermediate rate (0.28 kg-ai/ha) with the same treatment.

Shoot regrowth. There was significant (p < 0.05) three-way interaction among timing,

herbicide, and herbicide rate for the visual evaluation (Table 2-5). Only 2 glyphosate treatments

reduced shoot regrowth compared to the untreated controls (0.8 0.2 grams/pot); diflufenzopyr

applied 3 days after glyphosate (0.43 kg-ai/ha) and glyphosate alone (0.84 kg-ai/ha) (Table 2-7).

In each of these treatments the shoot regrowth more than doubled the biomass of the untreated

control. Glyphosate applied alone (0.43 and 0.84 kg-ai/ha) either yielded the most regrowth, or

did not differ from the treatment with the most regrowth within the rate; the other treatments

included diflufenzopyr applied 3 days after glyphosate (0.43 kg-ai/ha) or tank-mixed at 0.84 kg-

ai/ha. Diflufenzopyr had no effect on glyphosate at the highest rate (1.68 kg-ai/ha).

Four imazapyr treatments reduced cogongrass regrowth compared to the untreated control

(0.8 0.2 grams/pot); diflufenzopyr applied tank-mixed with any rate, or 3 days before imazapyr

(0.56 kg-ai/ha) (Table 2-7). Shoot regrowth was negligible when diflufenzopyr was tank mixed

with imazapyr (0.14 and 0.28 kg-ai/ha). While diflufenzopyr tank-mixed with imazapyr (0.28 kg-

ai/ha) yielded less regrowth compared to diflufenzopyr applied 3 days before or 3 days after,

imazapyr alone did not differ from any diflufenzopyr treatments. No effect was observed with

diflufenzopyr at the highest rate (0.56 kg-ai/ha)

Rhizome biomass. There was a significant (p < 0.05) two-way interaction between

herbicide and herbicide rate (Table 2-5). Timing was not significant when examined alone for

the rhizome biomass. No treatments reduced rhizome biomass compared to the untreated control

(8.2 6.4) (Table 2-8). Diflufenzopyr reduced rhizome biomass when applied with glyphosate

(0.84 kg-ai/ha) compared to glyphosate alone (Table 2-8). Applied tank-mixed or 3 days after









glyphosate (0.84 kg-ai/ha), diflufenzopyr reduced rhizome biomass compared to the same

treatment at the higher glyphosate rate (1.68 kg-ai/ha). Diflufenzopyr had no effect on rhizome

biomass when mixed with imazapyr.

Growth Regulator Study

Analysis of variance indicated a significant (p < 0.05) treatment by experiment interaction

for the shoot regrowth, therefore experiments are presented separately.

Experiment one

Overall model variance for experiment 2 parameters, including visual evaluation, shoot

regrowth biomass, and rhizome/root biomass are listed in Table 2-9.

Visual evaluation. There was a significant (p < 0.05) three-way interaction with growth

regulator, herbicide, and herbicide rate for the visual evaluation (Table 2-9). When applied in the

absence of glyphosate or imazapyr, < 20% control was observed for the PGR herbicides (Table

2-10). Although glyphosate control never exceeded 25% for the two lowest rates (0.43 and 0.84

kg-ai/ha), the addition of PGR herbicides had no effect on glyphosate. Glyphosate alone at 1.68

kg-ai/ha provided nearly 90% control. The addition of PGR herbicides to this rate of glyphosate

decreased control by greater than 50%.

Cogongrass control with imazapyr varied greatly (Table 2-10). Imazapyr applied alone,

regardless of rate, had < 30% control. Dicamba with imazapyr at the lowest rate (0.14 kg-ai/ha)

provided almost no observed control. Imazapyr (0.28 kg-ai/ha) with any PGR herbicide provided

nearly 70-90% control compared to imazapyr in the absence of PGR herbicides, although

dicamba did not differ from imazapyr alone. An even higher level of control was also observed

at any rate of imazapyr with 2,4-D. With the exception of 2,4-D, imazapyr treatments at the

highest rate (0.56 kg-ai/ha) did not exceed 65% control.









Shoot regrowth. There was a significant (p < 0.05) interaction among growth regulator,

herbicide, and herbicide rate for the shoot regrowth in experiment 2 (Table 2-9). While PGR

herbicides alone did not differ from the untreated control, triclopyr had less regrowth compared

to quinclorac. The addition of most PGR herbicides to glyphosate at the lowest rate (0.43 kg-

ai/ha) had no effect, with the exception of triclopyr. This triclopyr treatment tripled the amount

of shoot biomass compared to triclopyr alone and double the biomass compared to glyphosate

alone. Plant growth regulating herbicides also had no effect when glyphosate rate increased to

0.84 kg-ai/ha. Glyphosate alone at 1.68 kg-ai/ha reduced shoot regrowth to < 0.1 grams/pot. The

PGR herbicide treatments failed to provide this much reduction.

Overall, cogongrass regrowth with imazapyr was reduced compared to glyphosate

treatments (Table 2-12). Imazapyr alone did not differ from the untreated controls. Most

imazapyr treatments in conjunction with PGR herbicides provided < 0.4 grams of regrowth per

pot. Plant growth regulating herbicides with imazapyr at 0.28 kg-ai/ha reduced shoot regrowth

compared to imazapyr alone. Minimal shoot regrowth occurred with 2,4-D and imazapyr at the

lowest rate (0.14 kg-ai/ha), and almost no regrowth occurred at the higher rates (0.28 and 0.56

kg-ai/ha). Imazapyr and quinclorac had more shoot regrowth at the highest rate (0.56 kg-ai/ha)

compared to the 2 lower rates (0.14 and 0.28 kg-ai/ha).

Rhizome biomass. There was a high level of variability within experiment 1, resulting in

only significant (p < 0.05) distinction within PGR herbicides (Table 2-10). Majority of the

glyphosate or imazapyr treatments did not differ in rhizome biomass compared to the untreated

controls (Table 2-12). Triclopyr alone and glyphosate alone (1.68 kg-ai/ha) reduced rhizome

biomass. Imazapyr alone (0.28 and 0.56 kg-ai/ha), or imazapyr (0.28 kg-ai/ha) with 2,4-D or

quinclorac also reduced rhizome biomass compared to the untreated control. Rate of glyphosate









or imazapyr and most PGR herbicides had no effect on rhizome biomass compared to glyphosate

or imazapyr alone.

Experiment two

Overall model variance for experiment 2 parameters, including visual evaluation, shoot

regrowth biomass and rhizome/root biomass are listed in Table 2-13.

Visual evaluation. There was a significant (p < 0.05) three-way interaction with growth

regulator, herbicide, and herbicide rate for the visual evaluation (Table 2-13). When triclopyr

was applied in the absence of glyphosate or imazapyr almost no control was observed (Table 2-

14). Dicamba and quinclorac alone provide more control compared to untreated plants. The

remaining PGR herbicides alone did not differ from the untreated controls. No glyphosate

treatments exceeded 55% control. The effect of PGR herbicides was not observed at any rate of

glyphosate. Also, there was no difference between the level of control provided by the PGR

herbicides alone or in conjunction with glyphosate.

Similar, levels of control were observed with most imazapyr treatments, and many

treatments did not exceed 35% control (Table 2-14). However, imazapyr at the two highest rates

(0.28 and 0.56kg-ai/ha) with 2,4-D provided more control, almost 50% at 0.28 kg-ai/ha and

almost 90% at the highest imazapyr rate. Similar to glyphosate results, the level of control

provided by the PGR herbicides alone did not differ from the imazapyr/PGR herbicide

treatments, the exception being 2,4-D with the highest rate of imazapyr.

Shoot regrowth. There was a high level of variability within experiment 2 resulting in no

differences among treatments (Table 2-14). Only triclopyr with glyphosate at the lowest rate

(0.43 kg-ai/ha) yielded less shoot biomass compared to the untreated controls (Table 2-15).









Rhizome biomass. There was no significant (p < 0.05) interaction among growth

regulator, herbicide, and herbicide rate (Table 2-11). Also, no treatments reduced rhizome mass

compared to the untreated controls (Table 2-16).

Discussion

Acceptable cogongrass control is defined as having > 80% reduction in rhizome biomass 2

years after treatment (Willard et al. 1996). This level of control can best be achieved if the

management method targets the rhizomes and all viable tillers (Tanner et al. 1992, Willard et al.

1997). In these studies, growth regulating herbicides in conjunction with either glyphosate or

imazapyr targeted cogongrass rhizomes, to affect control. However, lack of consistent distinction

in rhizome dry weight for the diflufenzopyr timing experiments and the growth regulator

experiments leads to a closer examination of the visual evaluation and the shoot regrowth dry

weight. Thus, acceptable control, in this study, is defined as > 80% injury or visual reduction, 8

weeks after initial treatment.

Despite some of the discrepancies with both experiments in the diflufenzopyr timing study,

there are some consistent trends with the data. The best control in the diflufenzopyr study came

from imazapyr treatments (0.56 kg-ai/ha), which provided greater than 75% control with

diflufenzopyr. However, it was questionable whether diflufenzopyr made any difference with

these treatments in experiment 1. Extended control with imazapyr is common with cogongrass

management as a result of residual activity of the herbicide (Johnson et al. 1997, Willard et al.

1997). In experiment 1, imazapyr had acceptable control regardless of whether diflufenzopyr was

applied. However, in experiment 2, acceptable control was only achieved with imazapyr if

diflufenzopyr was included (> 90% control). Regardless of the experiment, imazapyr treatments

that were tank-mixed with diflufenzopyr yielded 0.1 grams of regrowth or less.









Glyphosate treatments provided unacceptable levels of regrowth control in both

experiments. Some glyphosate treatments at 0.43 and 0.84 kg-ai/ha actually increased shoot

regrowth when applied alone, compared to some diflufenzopyr applications. Increased growth is

a symptom that, although rare, sometimes follows a glyphosate application (Marrs et al. 1989).

As there is no prior documentation of discrepancies using diflufenzopyr, the

inconsistencies in the diflufenzopyr experiments could have occurred as a result of experimental

timing. Experiment 1 occurred in the fall, whereas experiment 2 occurred in the spring. While

both of the experiments occurred in a temperature controlled greenhouse, inconsistent artificial

light, caused by a faulty light system, may have been the problem. It is possible that

experimental differences occurred as a result of day-length, even if only for a short period. Day-

length is just one of the factors responsible for translocation of photosynthates in the leaves

down to the rhizomes in preparation for winter dormancy (Gaffney 1996). Herbicide applications

in the fall tend to result in greater efficacy compared to spring treatments (> 20% more control,

12 months after treatment) for both glyphosate and imazapyr as they are actively translocated

with the photosynthates to the rhizomes (Tanner et al. 1992, Gaffney 1996, Johnson et al. 1997).

The growth regulator study indicated imazapyr (0.56 kg-ai/ha) and 2,4-D provided

approximately 90% control or greater. This treatment decreased shoot regrowth when compared

to untreated plants. Collectively, these experiments suggest the addition/combination of dicamba,

quinclorac, or triclopyr with glyphosate or imazapyr for cogongrass control does not provide any

advantage. The advantage of adding/combining PGR herbicides to glyphosate or imazapyr was

only observed with imazapyr in conjunction with 2,4-D or diflufenzopyr. However, the overall

inconsistencies may be due to an insufficient interval to increase shoot:rhizome ratio, a problem









that is addressed in the field study. Other explanations include a decrease in translocation or

general inconsistencies with the PGR herbicides.

Table 2-1. Overall model variance for the visual evaluation, shoot regrowth biomass, and
rhizome biomass 8 weeks after initial treatment in the cogongrass diflufenzopyr
timing Experiment 1.
Visual evaluation Shoot regrowth Rhizome
Variables p-value p-value p-value
Experiment1 < 0.0001 < 0.0001 < 0.0001
Timing < 0.0001 < 0.0001 0.0880
Herbicide < 0.0001 < 0.0001 0.8797
Timing*herbicide 0.4016 0.0004 0.2406
Herbicide rate < 0.0001 < 0.0001 0.0886
Timing*herbicide rate 0.0026 0.0350 0.0865
Herbicide*herbicide rate < 0.0001 < 0.0001 0.2860
Timing*herbicide*herbicide rate 0.0070 0.0585 0.3139
Rep 0.9653 0.7309 0.4316
.Experiment comparison between experiment 1 and experiment 2 for the cogongrass
diflufenzopyr study.

Table 2-2. Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
in Experiment 1.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)
Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56
% Control
Absent 0 0.1 0 +0 60 18 80 8 93 6 98 6
3 days prior 5 10 20 22 55 26 95 6 98 6 100 +0
Tank-mix 48 32 38 30 35 26 95 6 98 6 100 +0
3 days after 8 10 0 + 0 68 22 88 10 95 6 95 6
1Means followed by 95% confidence interval.

Table 2-3. Cogongrass shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
in Experiment 1.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)
Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56
Grams/pot
Absent 1.7 0.8.1. 1.6 0.4 0.4 0.4 0.1 +0 < 0.1 0 < 0.1 0
3 days prior 1.0 +0.6 0.7 0.4 0.4 0.4 < 0.10 < 0.10 < 0.1 0
Tank-mix 0.3 0.2 0.6 0.6 0.3 0.2 < 0.1 0 < 0.1 0 < 0.1 0
3 days after 1.2 0.6 1.2 0.2 0.2 0.2 < 0.10 < 0.10 < 0.1 0
.Means followed by 95% confidence interval.









Table 2-4. Cogongrass rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
in Experiment 1.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)


Diflufenzopyr
timing


0.43


0.84


Absent 9.6 1.41 11.6 + 2.8
3 days prior 7.7 + 0.6 4.1+ 1.2
Tank-mix 3.6 2.0 6.0 3.6
3 days after 7.8 2.6 7.2 2.2
1Means followed by 95% confidence interval.


1.68 0.14
Grams/pot
5.7 3.4 9.5
6.2 + 3.4 6.9
7.0 + 1.2 7.4
7.2 2.0 10.1


Table 2-5. Overall model variance for the visual evaluation, shoot regrowth biomass, and
rhizome biomass 8 weeks after initial treatment in the cogongrass diflufenzopyr
timing Experiment 2.
Visual evaluation Shoot regrowth Rhizome
Variables p-value p-value p-value
Experiment1 < 0.0001 < 0.0001 < 0.0001
Timing 0.0013 0.2927 0.7981
Herbicide < 0.0001 < 0.0001 < 0.0001
Timing*herbicide < 0.0001 0.0335 0.2406
Herbicide rate 0.1004 0.9424 0.1719
Timing*herbicide rate 0.3764 0.1210 0.1562
Herbicide*herbicide rate 0.0117 0.0165 0.0446
Timing*herbicide*herbicide rate 0.0478 0.0016 0.0540
Rep 0.7654 0.7215 0.8715
.Experiment comparison between experiment 1 and experiment 2 for the cogongrass
diflufenzopyr study.

Table 2-6. Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
in Experiment 2.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)
Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56


Absent 40 14.1 10 8
3 days prior 45 12 40 16
Tank-mix 33 6 30 24
3 days after 23 18 35 10
1Means followed by 95% confidence interval.


28 6
38 28
13 16
30 24


% Control
35 30 53 44
45 10 38 18
90 + 8 95 10
60 14 30 14


50 + 40
90 12
98 6
75 + 30


0.28


+ 1.6
+ 2.8
+ 2.4
+ 3.4


6.5 4.4
7.3 1.4
6.1 4.8
6.0 1.6


0.56

4.5 2.8
3.9 0.8
7.5 3.6
6.9 3.8


I









Table 2-7. Cogongrass shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
for Experiment 2.
Glyphosate (kg-ai/ha). Imazapyr (kg-ai/ha)
Diflufenzopyr
timing 0.43 0.84 1.68 0.14 0.28 0.56
Grams/pot
Absent 1.0 1.0.. 2.0+ 0.4 1.4 0.8 1.0+ 0.4 0.4 0.4 0.8 0.8
3 days prior 1.0 + 0.4 1.1 0.4 1.3 0.8 1.0 + 0.4 1.0 + 0.6 0.1 0.2
Tank-mix 1.0 +0.2 1.1 0.6 2.2 1.0 0.1 0.2 <0.10 < 0.1 0
3 days after 2.1 + 0.4 0.7 + 0.4 1.7 + 1.4 0.5 0.4 0.9 + 0.4 0.4 0.6
.Means followed by 95% confidence interval.

Table 2-8. Cogongrass rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
for Experiment 2.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)


Diflufenzopyr
timing


0.43


0.84


1.68


0.14


0.28


0.56


Absent 3.2 2.2' 10.6 5.6
3 days prior 3.9 2.0 3.6 + 1.6
Tank-mix 4.9 2.6 3.7 + 1.2
3 days after 9.1 4.4 2.4 1.0
.Means followed by 95% confidence interval.


Grams/pot
7.7 7.2 3.6 1.6
7.1 5.4 4.2 2.4
11.2 5.8 3.7 2.6
9.0 2.4 2.5 1.8


Table 2-9. Overall model variance for the visual evaluation, shoot regrowth biomass, and
rhizome biomass 8 weeks after initial treatment in the cogongrass growth regulator
Experiment 1.
Visual evaluation Shoot regrowth Rhizome
Variables p-value p-value p-value
Experiment1 0.0812 0.0014 0.9471
Growth regulator < 0.0001 0.0179 0.0799
Herbicide < 0.0001 < 0.0001 0.6256
Growth regulator*herbicide < 0.0001 0.0101 0.3549
Rate < 0.0001 0.0657 0.2569
Growth regulator* herbicide rate < 0.0001 < 0.0001 0.4292
Herbicide*herbicide rate < 0.0001 0.0018 0.4679
Growth regulator*herbicide*herbicide rate 0.0045 0.0247 0.1147
Rep 0.2629 0.3550 0.9058
1Experiment comparison between experiment 1 and experiment 2 for the cogongrass growth
regulator study.


2.1 + 1.4
5.6 4.8
1.5 0.8
2.3 0.8


3.6 1.0
5.6 4.8
2.6 1.4
2.8 1.4









Table 2-10. Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by plant growth regulating herbicides
in Experiment 1.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)
Growth regulator Control. 0.43 0.84 1.68 0.14 0.28 0.56
% Control
Absent 0 02 23 12 5 6 88 10 25 20 20 20 28 26
2,4-D 15 6 13 10 18 28 23 26 78 10 90 + 8 100 + 0
Dicamba 10+ 0 10 + 8 8 10 25 20 5 8 68 30 40 32
Quinclorac 0 + 0 20 20 13 10 28 48 38 10 75 32 20 + 8
Triclopyr 15 10 5 6 10 14 25 20 30 22 90 12 63 20
1~ 2
.Growth regulating herbicides applied alone in absence of glyphosate or imazapyr.. Means
followed by 95% confidence interval.

Table 2-11. Cogongrass shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by plant growth regulating herbicides
in Experiment 1.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)
Growth
regulator Control. 0.43 0.84 1.68 0.14 0.28 0.56
Grams/pot
Absent 1.0 + 0.42 0.8 0.0 1.0 + 0.6 <0.1 + 0 0.7 0.2 0.7 0.2 0.5 0.4
2,4-D 0.7 1.2 0.7 0.2 1.3 0.2 0.5 0.2 0.2 0.0 <0.1 0 <0.1 0
Dicamba 0.8 0.2 0.7 0.2 1.5 0.8 0.6 0.4 1.1 0.4 0.2 0.2 0.3 0.2
Quinclorac 1.2 0.4 0.9 0.6 0.8 0.4 1.6 1.4 0.4 0.2 0.2 0.2 0.9 0.2
Triclopyr 0.5 0.2 1.6 0.6 1.0 + 0.8 0.7 0.6 0.4 0.2 0.1 0.0 0.2 0.2
.Growth regulating herbicide applied alone in absence of glyphosate or imazapyr. 2Means
followed by 95% confidence interval.

Table 2-12. Cogongrass rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by plant growth regulating herbicides
in Experiment 1.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)
Growth
regulator Control. 0.43 0.84 1.68 0.14 0.28 0.56
Grams/pot
Absent 6.1 2.22 4.0 2.6 4.0 + 0.6 0.9 0.6 4.0 1.8 2.2 0.2 2.9 0.2
2,4-D 4.3 3.8 3.6 1.2 4.3 3.6 4.6 3.6 3.5 2.8 3.7 1.0 3.1 1.8
Dicamba 3.4 1.8 5.7 4.4 4.8 3.6 4.5 1.2 7.6 3.0 4.7 3.4 3.2 2.0
Quinclorac 6.9 2.4 5.1 2.8 4.3 14.6 7.3 4.0 5.9 3.6 2.8 1.4 5.5 2.2
Triclopyr 3.0 + 0.6 7.9 6.8 5.5 3.4 3.5 2.2 3.1 2.6 3.3 3.2 7.9 5.2
.Growth regulating herbicide applied alone in absence of glyphosate or imazapyr. 2Means
followed by 95% confidence interval.









Table 2-13. Overall model variance for the visual evaluation, shoot regrowth biomass, and
rhizome biomass 8 weeks after initial treatment in the cogongrass growth regulator
Experiment 2.


Visual evaluation Shoot regrowth
p-value p-value


Variables


Rhizome
p-value


Experiment1 0.0812 0.0014 0.9471
Growth regulator < 0.0001 0.1589 0.3652
Herbicide 0.0449 0.8143 0.4313
Growth regulator*herbicide 0.0026 0.0596 0.0538
Rate 0.0025 0.1310 0.0536
Growth regulator* herbicide rate 0.0749 0.9698 0.8537
Herbicide*herbicide rate 0.0748 0.1386 0.9968
Growth regulator*herbicide*herbicide rate 0.0235 0.4928 0.4309
Rep 0.9945 0.8581 0.9764
.Experiment comparison between experiment 1 and experiment 2 for the cogongrass growth
regulator study.

Table 2-14. Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influences by plant growth regulating herbicides
in Experiment 2.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)
Growth regulator Control. 0.43 0.84 1.68 0.14 0.28 0.56
% Control
Absent 0 + 02 30 18 18 10 15 6 23 18 20 16 35 12
2,4-D 38 6 33 6 25 18 30 14 25 20 48 6 88 18
Dicamba 25 20 20 14 28 18 35 10 28 10 20 14 30 22
Quinclorac 30 + 8 43 10 35 24 53 34 35 12 18 12 25 10
Triclopyr 10 12 25 10 20 12 25 18 15 6 20 18 35 32
1Growth regulating herbicides applied alone or in the absence of glyphosate or imazapyr.
2Means followed by 95% confidence interval.

Table 2-15. Cogongrass shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influences by plant growth regulating herbicides
in Experiment 2.


Glyphosate (kg-ai/ha)


Imazapyr (kg-ai/ha)


Growth
regulator


Control1 0.43 0.84


1.68


0.14


0.28


0.56


Grams/pot
Absent 1.4 0.42 0.8 0.8 1.1 0.0 1.1 0.4 1.1 0.8 1.7 2.4 0.7 0.4
2,4-D 0.5 0.2 0.9 0.4 1.3 1.0 1.2 0.8 1.1 0.6 0.5 0.0 0.2 0.2
Dicamba 0.7 0.4 1.0 +0.4 0.9 0.6 0.6 0.2 1.0 +0.6 1.2 0.6 0.8 0.4
Quinclorac 0.7 0.2 0.6 0.2 0.4 0.2 0.5 0.4 0.7 0.4 1.5 0.8 0.7 0.4
Triclopyr 1.8 0.8 0.7 0.2 1.0 + 0.4 1.0 + 0.6 1.3 0.8 1.0 + 0.6 0.6 0.4
1Growth regulating herbicides applied alone or in the absence of glyphosate or imazapyr.
2Means followed by 95% confidence interval.









Table 2-16. Cogongrass rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influences by plant growth regulating herbicides
in Experiment 2.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)
Growth
regulator Control. 0.43 0.84 1.68 0.14 0.28 0.56
Grams/pot
Absent 5.9 2.22 5.3 4.6 6.6 1.6 5.0 1.0 4.6 2.6 4.5 3.4 2.7 0.6
2,4-D 2.9 1.2 4.8 0.8 6.8 4.8 5.5 2.4 4.1 2.0 3.2 1.2 3.5 0.6
Dicamba 3.9 2.4 7.6 6.4 6.5 3.6 3.5 1.4 5.3 1.8 4.3 1.6 3.3 2.2
Quinclorac 3.5 2.2 3.7 1.0 2.5 1.8 2.0 1.2 3.8 1.4 7.7 3.4 3.0 1.8
Triclopyr 6.3 2.6 4.7 1.2 4.7 1.6 3.1 + 1.2 5.3 2.8 4.2 1.6 2.8 1.0
.Growth regulating herbicides applied alone or in the absence of glyphosate or imazapyr.
2Means followed by 95% confidence interval.









CHAPTER 3
THE INFLUENCE OF GROWTH REGULATOR HERBICIDES ON THE EFFICACY OF
GLYPHOSATE AND IMAZAPYR ON TORPEDOGRASS UNDER GREENHOUSE
CONDITIONS

Introduction

Torpedograss is an old world Eurasian plant and is most frequently found near or in

aquatic sites (Holm et al. 1977). Since 1992, Florida Department of Environmental Protection

has ranked torpedograss as the 2nd most abundant plant in Florida lakes (Schardt 1992, Schardt

personal communication, February 2007). Torpedograss can also be found on terrestrial areas

such as golf courses and roadsides (McCarty et al. 1993). The presence of torpedograss is

problematic in Florida because it interrupts flood control, irrigation and turf production (Shilling

and Haller 1989, McCarty et al. 1993).

The rapid growth and extensive rhizome system are the primary issues with torpedograss'

invasiveness. The rhizome system comprises 70 to 90% of total biomass (Smith et al. 1999).

When fragmented, 92 to 96% of rhizome buds can regenerate when temperatures range from 20

to 35C (Hossain et al. 2001). New buds are continuously produced along the entire length of the

rhizomes indicating very weak apical dominance (Wilcut et al. 1988a). Since all of the nodes

found on the rhizome system can be viable, complete control of torpedograss requires total

removal of all viable tillers and rhizomes (Sutton 1996, Smith et al. 1999).

Most torpedograss management studies come with mixed success, with few showing 100%

long term control (> 12 months) within time constraints and budgets for the average landowner

(Manipura and Somaratne 1974, Willard et al. 1998, Smith et al. 1999). Studies have most

commonly used glyphosate and imazapyr for torpedograss control (Baird et al. 1983, Shilling

and Haller 1989, Willard et al. 1998, Smith et al. 1999, Hanlon and Langeland 2000).









Long term control (>12 months) has never been reported for torpedograss using glyphosate

[N-(phosphonomethyl)glycine] with a single application (Manipura and Somaratne 1974,

Shilling and Haller 1989, Smith et al. 1999). Limited control from glyphosate is often attributed

to the aquatic habitat of torpedograss as the herbicide only reaches the emergent portion of the

plant. Although the emergent portion of the plant was controlled, regrowth from rhizomes and

submerged stems segments occurred within a few months (Baird et al. 1983). Smith et al. (1999)

concluded that high water levels inhibit foliar interception of glyphosate and control correlated

with foliar exposure to water level ratio. To achieve > 90% control (5 weeks after initial

treatment), a glyphosate application rate of 2.24 kg-ai/ha was needed to be intercepted by at least

40% of the foliage. Lower rates correlated with a higher percentage of foliage cover to achieve

similar results (Smith et al. 1999).

Imazapyr applications on torpedograss have shown similar issues with submergence and in

turn, less control (Hanlon and Langeland 2000). Inconsistencies in data presented by Hanlon and

Langeland (2000) lead the authors to speculate that fluctuating water depth at different

experimental sites could have influenced results. While all experiments began in approximately

0.8 meters of water, by the end of the experiment, one study site was considered dry while the

remaining sites were flooded. Greater than 95% control was observed at the dry site and < 25%

control for the flooded sites. The authors also speculated that thatch levels may have contributed

to inconsistent control as the amount of torpedograss tissue exposed to the herbicide may be

reduced. This reduction may have been a result of thatch preventing the herbicide from achieving

adequate uptake (Hanlon and Langeland 2000).

Collectively, results from previous studies indicate poor control of torpedograss with a low

percentage of exposed foliar tissue. Therefore, methods to increase control are highly warranted.









If torpedograss rhizomes could be chemically stimulated to increase shoot production, allowing

more of the plant to be exposed, then herbicide applications of glyphosate or imazapyr could

potentially be more effective.

Increased shoot production has been accomplished using growth regulating herbicides,

such as dicamba on wheat, Triticum aestivum (Bahieldin et al. 2000). These herbicides interfere

with growth hormone functions and have similar modes of action and selectivity (Anderson

1996). Although the true mode of action for some of these herbicides is unknown, it is speculated

that some mimic auxins in an unregulated fashion in plants, while others block the transport of

auxins (Anderson 1996, WSSA 2002, Lym and Deibert 2005).

Several herbicides interfere with normal auxin function in plants. These include not only

dicamba, but also triclopyr, 2,4-D, quinclorac, and diflufenzopyr, as well as others (Anderson

1996, WSSA 2002). Previous research by English (1998) studied the impact of these herbicides

on bud break in cogongrass and found that diflufenzopyr was most effective on other invasive

grasses, such as cogongrass.

Application timing of diflufenzopyr appears to be critical for control (Ketchersid and

Senseman 1998). The combination of diflufenzopyr and dicamba proved more phytotoxic to

other broadleaves such as field bindweed (Convovulus arvense L.) and velvetleaf (Abutilon

theophrasti Medic.) when diflufenzopyr was applied 3 days before the herbicide compared to

diflufenzopyr in conjunction with or after application (Ketchersid and Senseman 1998).

Since torpedograss occurs in aquatics, an area where most control methods are not feasible

or may be ineffective; the use of growth regulating herbicides in conjunction with current control

methods warrants research. The application timing of diflufenzopyr and the combination of

glyphosate or imazapyr with growth regulating herbicides has never been studied on









torpedograss. Thus, this study has two objectives: 1.) determine the effect of diflufenzopyr

application timing on the efficacy of glyphosate and imazapyr on torpedograss, and 2.) determine

the effect of growth regulating herbicides, other than diflufenzopyr, on the efficacy of glyphosate

and imazapyr on torpedograss.

Materials and Methods

Torpedograss plants were established from rhizomes that were obtained from local

Gainesville populations. Plants were grown under greenhouse conditions with the following

environmental parameters: 12 hr day, 12 hr night, temperature 30/20C. Torpedograss was grown

in 3L pots with commercial potting soil.3 and amended with slow-release fertilizer.4.

Plants were grown for 8 to 10 weeks to ensure a dense and healthy rhizome mass.

Treatments for both studies were applied using a standard small plot sprayer with appropriate

nonionic surfactant (0.25% v/v) and a spray volume of 187L/ha. Shoot biomass was removed 4

weeks after initial treatment (WAIT) and plants were then allowed to regrow for 4 weeks. After

this time period, visual assessments (0 = no control, 100 = complete control) on shoot regrowth

were performed and shoot regrowth and root biomass were collected. Samples were placed in a

forced air oven at 70 C for 3 days and dry weights recorded.

Diflufenzopyr Timing Study

This study was a 4 (diflufenzopyr timings) by 2 (glyphosate or imazapyr) by 4 (rates)

factorial in a completely randomized design. Diflufenzopyr was selected specifically for this

study because it has been determined through research by English (1998) and Gaffney (1996) to

have caused a greater level bud break in other invasive grasses, such as cogongrass. Treatments

for this study included diflufenzopyr applied at a rate of 0.22 kg-ai/ha 3 days prior, in

3 Metro mix Agricultural Lite Mix
4 Scotts. Osmocote 14-14-14









conjunction with, or 3 days after the application of glyphosate or imazapyr. Glyphosate and

imazapyr rates included 0.0, 0.43, 0.84, or 1.68 kg-ai/ha and 0.0, 0.14, 0.28, or 0.56 kg-ai/ha,

respectively. Three diflufenzopyr timings were chosen because it is uncertain when axillary

shoot growth will be stimulated with diflufenzopyr. Controls consisted of untreated plants, only

surfactant treatment, and diflufenzopyr alone treatments. Experiment one occurred from 2

February 2006 to 10 April 2006 and experiment two occurred from 20 March 2006 to 15 May

2006.

Growth Regulator Study

This study was a 4 (growth regulating herbicides) by 2 (glyphosate or imazapyr) by 4

(rates) factorial in a completely randomized design. In this study, PGR herbicides were applied

to actively growing cogongrass in conjunction with glyphosate and imazapyr. The rates for

dicamba, 2,4-D, triclopyr, and quinclorac were 0.56, 1.12, 0.56, and 1.4 kg-ai/ha, respectively.

The glyphosate and imazapyr rates were the same as reported for study one. Experiment one

occurred from 7 March 2006 2 May 2006 and experiment two occurred from 10 May 2006 5

July 2006.

Statistical Analysis

Data were analyzed using proc GLM program in SAS 9.1. Models for the independent

variables (experiment, growth regulating herbicides or timing, herbicide, and rate) were

determined using the dependent variables (visual evaluations, and shoot regrowth and

rhizome/root biomass harvests). Data are reported as p-values for interaction and means with

95% confidence intervals for statistical difference. All studies were conducted twice with 4

replications.









Results


Diflufenzopyr Timing Study

Analysis of variance indicated a significant treatment by experiment interaction therefore

experiments are presented separately.

Experiment one

Visual evaluation. There was significant (p < 0.05) three-way interaction with timing,

herbicide, and herbicide rate for the visual evaluation (Table 3-1). Glyphosate treatments did not

exceed 50% control (Table 3-2). No effect was observed by adding diflufenzopyr to glyphosate

at the lowest and highest rates (0.43 and 1.68 kg-ai/ha). Diflufenzopyr applied to glyphosate at

0.84 kg-ai/ha either decreased the level of control provided by glyphosate alone or did not differ

from it. A rate effect was observed when diflufenzopyr was applied 3 days before glyphosate.

The lowest rate (0.43 kg-ai/ha) had more control compared to the 2 highest rates (0.84 and 1.68

kg-ai/ha).

Torpedograss control also never exceeded 50% with imazapyr treatments (Table 3-2). The

addition of diflufenzopyr to imazapyr at 0.14 and 0.56 kg-ai/ha had no effect. Diflufenzopyr

when tank-mixed with imazapyr at 0.28 kg-ai/ha exceeded the level control observed when it

was applied 3 days after. However, no treatments differed from imazapyr alone.

Shoot regrowth. There was significant (p < 0.05) two-way interaction with herbicide and

herbicide rate, but no three-way interaction (Table 3-1). Timing was also a significant (p < 0.05)

when examined alone. No treatments reduced shoot regrowth compared to the untreated controls

(0.8 + 0.2 grams/pot) (Table 3-3). Diflufenzopyr had no effect on the shoot regrowth with

glyphosate at 0.43 and 0.84 kg-ai/ha, or imazapyr at any rate. When glyphosate (1.69 kg-ai/ha) or

imazapyr (0.28 kg-ai/ha) were tank-mixed with diflufenzopyr, 50% less shoot regrowth occurred

compared to when diflufenzopyr was applied 3 days after glyphosate or imazapyr.









Rhizome biomass. There was significant (p < 0.05) two-way interaction with herbicide

and herbicide rate, but no three-way interaction (Table 3-1). Timing was also a significant (p <

0.05) when examined alone. Rhizome biomass was reduced with only 3 treatments, compared to

the untreated control (3.4 + 1.6 grams/pot). These treatments included glyphosate alone (0.84 kg-

ai/ha), imazapyr alone (0.28 kg-ai/ha), and diflufenzopyr applied 3 days before glyphosate (1.68

kg-ai/ha). Diflufenzopyr with glyphosate (0.43 kg-ai/ha) increased the rhizome biomass

compared to glyphosate alone. No effect was observed with diflufenzopyr as glyphosate rate

increased to 0.84 kg-ai/ha. When diflufenzopyr was applied 3 days after glyphosate at 1.68 kg-

ai/ha rhizome biomass more than doubled in comparison to the remaining treatments at this rate.

Torpedograss rhizome biomass was not affected by the addition of diflufenzopyr to

imazapyr at 0.14 kg-ai/ha. Imazapyr alone reduced rhizome mass in comparison to diflufenzopyr

applied 3 days before or 3 days after. Diflufenzopyr tank-mixed with imazapyr at 0.56 kg-ai/ha

reduced rhizome mass compared to imazapyr alone. A rate effect was observed with imazapyr

alone. The intermediate rate (0.28 kg-ai/ha) had greater rhizome mass compared to the highest

and the lowest rates.

Experiment two

Overall model variance for experiment 2 parameters, including visual evaluation, shoot

regrowth biomass, and rhizome/root biomass are listed in Table 3-7.

Visual evaluation. There was no two- or three-way interaction for the visual evaluation

(Table 3-7). However, herbicide rate was significant (p < 0.05) when examined alone.

Diflufenzopyr had no effect in this experiment. Most treatments provided the same level of

control at any rate. When diflufenzopyr was applied 3 days before glyphosate, the lowest

glyphosate rate (0.14 kg-ai/ha) provided more control compared to the highest rate (1.65 kg-

ai/ha)









Shoot regrowth. There was a high level of variability within experiment 2, resulting in no

differences among treatments (Table 3-7). Also, no treatments reduced shoot regrowth compared

to the untreated control (0.7 0.4) (Table 3-7).

Rhizome biomass. There was no two- or three-way interaction for the visual evaluation

(Table 3-5). However, herbicide was significant (p < 0.05) when examined alone. Only 3

treatments reduced rhizome mass compared to the untreated control (4.3 0.6 grams/pot);

diflufenzopyr applied 3 days before glyphosate (0.14 kg-ai/ha), tank mixed with glyphosate at

0.84 kg-ai/ha, and diflufenzopyr applied 3 days after imazapyr (0.28 kg-ai/ha) (Table 3-8).

Diflufenzopyr had no effect on rhizome biomass when combined with glyphosate at the 2 highest

rates (0.84 and 1.68 kg-ai/ha) or with imazapyr at the 2 lowest rates (0.14 and 0.28 kg-ai/ha).

When diflufenzopyr was applied 3 days before glyphosate (0.14 kg-ai/ha) rhizome biomass was

reduced compared to glyphosate alone. A reduction in rhizome biomass was also observed when

diflufenzopyr was tank-mixed or applied 3 days after imazapyr at 0.56 kg-ai/ha compared to

imazapyr alone.

Growth Regulator Study

Overall, model variance for experiment 1 parameters, including visual evaluation, shoot

regrowth biomass and rhizome/root biomass are listed in Table 3-9.

Experiment one

Visual evaluation. There was a significant (p < 0.05) three-way interaction with growth

regulator, herbicide, and herbicide rate interaction for the visual evaluation (Table 3-9). When

PGR herbicides were applied in the absence of glyphosate or imazapyr control did not differ

from the untreated plants (Table 3-10). Glyphosate control never exceeded 40%, and the addition

of PGR herbicides had no effect. There also appears to be a rate effect with the highest rate of

glyphosate (1.68 kg-ai/ha) and dicamba, compared to the lowest rate (0.43 kg-a/ha).









The effect of PGR herbicides with imazapyr was not observed at the 2 lowest rates (0.14

and 0.28 kg-ai/ha) (Table 3-10). The highest rate of imazapyr (0.56 kg-ai/ha) with 2,4-D

provided the most control, 75%. The remaining PGR herbicides had no effect on the level of

control provided by imazapyr at that rate.

Shoot regrowth. There was a significant (p < 0.05) three-way interaction among growth

regulator, herbicide, and herbicide rate for the visual evaluation (Table 3-9). Plant growth

regulating herbicides applied alone did not differ from the untreated controls (Table 3-11). In

fact, only 4 treatments overall differed from these untreated plants, glyphosate at 0.84 kg-ai/ha

with dicamba or quinclorac, and imazapyr at 0.56 kg-ai/ha with quinclorac, all increasing the

shoot regrowth biomass. The only treatment that decreased shoot biomass compared to the

untreated controls was imazapyr at the highest rate (0.56 kg-ai/ha) with 2,4-D. This treatment

also yielded less shoot regrowth compared to 2,4-D with the lowest rate of imazapyr. Glyphosate

treatments (0.84 kg-ai/ha) with dicamba or quinclorac increased shoot regrowth compared to

when they were applied with the lowest and highest glyphosate rates (0.14 and 1.68 kg-ai/ha).

However, dicamba with glyphosate at 0.43 kg-ai/ha did not differ from either of the 2 higher

rates. By adding glyphosate or imazapyr to the PGR herbicides, the level of control did not differ

from the PGR herbicides alone, with the exception of 2,4-D and imazapyr at 0.56 kg-ai/ha.

Rhizome biomass. There was no significant (p < 0.05) interaction among variables. (Table

3-9). Also, no treatments reduced rhizome biomass compared to the untreated control (Table 3-

12).

Experiment two

Overall model variance for experiment 2 parameters, including visual evaluation, shoot

regrowth biomass and rhizome/root biomass are listed in Table 3-13.









Visual evaluation. There was a significant (p < 0.05) two-way interaction with growth

regulator and herbicide rate, but no three-way interaction (Table 3-13). The variable herbicide

was not significant. All treatments in this experiment did not differ from control provided by the

untreated plants (Table 3-14). The effect of the PGR herbicides was not observed for the 2

highest rates of glyphosate (0.84 and 1.68 kg-ai/ha) or with imazapyr at 0.56 kg-ai/ha. Dicamba

with glyphosate (0.43 kg-ai/ha) provided almost 75% control, and was higher in comparison to

imazapyr alone, 20%. The greatest level of control observed with imazapyr at 0.14 kg-ai/ha

occurred with 2,4-D, dicamba, and triclopyr. Control with imazapyr at 0.28 kg-ai/ha was greatest

with dicamba or triclopyr compared to quinclorac at this rate, but these treatments did not differ

from imazapyr alone.

Shoot regrowth. There was a high level of variability within experiment 2, resulting in no

differences among treatments (Table 3-15) Also, no treatments reduced shoot regrowth

compared to the untreated control (Table 3-14).

Rhizome biomass. There was a high level of variability within experiment 2, resulting in

no differences among treatments (Table 3-15). Also, no treatments reduced rhizome biomass

compared to the untreated control (Table 3-16).

Discussion

Acceptable control is defined as having > 80% reduction in rhizome mass 2 years after

treatment, on a similar rhizomatous invasive plant, cogongrass (Willard et al. 1996). This level of

control can best be achieved on torpedograss if the management method targets the rhizomes and

all viable tillers (Sutton 1996, Smith et al. 1999). In this experiment, the rhizomes were targeted

using PGR herbicides and either glyphosate or imazapyr. Only one treatment, diflufenzopyr

applied tank-mixed with imazapyr (0.56 kg-ai/ha), provided consistent reduction in rhizome

biomass compared to imazapyr alone. However, overall lack of consistent distinction in rhizome









dry weight for the diflufenzopyr timing experiment and the growth regulator experiment leads to

a closer examination of the visual evaluation and the shoot regrowth dry weight. Thus,

acceptable control, in this study, is defined as > 80% injury or visual reduction, 8 weeks after

initial treatment.

In the timing study, acceptable control was not achieved, regardless of treatment. However,

shoot regrowth decreased when diflufenzopyr was applied 3 days before glyphosate (0.43 kg-

ai/ha) for experiment 1 when compared to glyphosate alone. This treatment also reduced rhizome

biomass. Overall, however, rhizome data indicate that rhizome biomass was reduced more often

with glyphosate or imazapyr treatments tank-mixed with diflufenzopyr in either study. Findings

by Ketchersid and Senseman (1998) suggested that diflufenzopyr was more phytotoxic to

broadleaf plants when applied 3 days before a dicamba application. While this was true for one

treatment that decreased shoot regrowth, rhizome data are not consistent with these findings.

These differing results may be due to different target weeds; Ketchersid and Senseman (1998)

targeted broadleaf weeds, whereas this experiment targeted torpedograss, a grass. Differing

results may also be due to different diflufenzopyr tank-mixes.

Acceptable control was also not achieved in the growth regulator experiment and results

were inconsistent. Similar to the visual evaluation data, shoot regrowth and rhizome dry weight

patterns were inconsistent. Also observed with the PGR herbicide treatment was the overall lack

of control that was achieved using quinclorac; a registered herbicide for torpedograss in turf

grass (Anonymous 2006). Quinclorac when applied with glyphosate (0.84 kg-ai/ha) in

experiment 1, actually increased shoot regrowth compared to the highest and the lowest rates.

Although not documented with glyphosate, an increase in shoot regrowth by quinclorac alone

was also observed by Busey (2003), who indicated that the torpedograss canopy increased after









the initial reduction by quinclorac in a multi-application treatment. Several studies indicate that

multiple applications are necessary to achieve acceptable control (McCarty et al. 1993, Busey

2003). McCarty et al. (1993) concluded that quinclorac applications at 2.2 kg-ai/ha followed by

1.1 kg-ai/ha 3 and 6 weeks after initial treatment (WAT) could control torpedograss (85-90%

control) for a short time, 7-10 WAIT. Busey (2003) found 4 applications at 0.42 kg-ai/ha per

year for 2 years reduced torpedograss dry weight 80%.

While this study did not provide long term results, it did provide initial expectations within

a short period of time. The advantage of adding/combining PGR herbicides to glyphosate or

imazapyr was not observed. The overall inconsistencies may be due to a decrease in

translocation or general inconsistencies with the PGR herbicides. Inconsistencies from this study

are readdressed in the field study, where results are indicative of real-world situations.

Table 3-1. Overall model variance for the visual evaluation, shoot regrowth biomass, and
rhizome biomass 8 weeks after initial treatment in the torpedograss diflufenzopyr
timing Experiment 1.
Visual evaluation Shoot regrowth Rhizome
Variables p-value p-value p-value
Experiment1 < 0.0001 < 0.0001 < 0.0001
Timing 0.2910 0.0130 0.0096
Herbicide 0.4024 0.3816 0.0261
Timing*herbicide 0.7330 0.2055 0.2659
Rate 0.4031 0.1103 0.3833
Timing*herbicide rate 0.3731 0.9476 0.8039
Herbicide* herbicide rate 0.1263 0.0354 0.0469
Timing*herbicide* herbicide rate 0.0130 0.1332 0.6624
Rep 0.7698 0.9323 0.6630
.Experiment comparison between experiment 1 and experiment 2 for the torpedograss
diflufenzopyr study.









Table 3-2. Percent control of torpedograss regrowth 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
in Experiment 1.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)
Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56
% Control
Absent 40+ 26.1 45 26 18 22 38 20 23 26 30 16
3 days prior 50 + 0 10 + 8 13 12 20 24 28 24 43 26
Tank-mix 18 18 23 10 33 12 35 18 43 18 18 16
3 days after 30 + 8 13 10 15 12 18 12 13 10 40 34
.Means followed by 95% confidence interval.

Table 3-3. Torpedograss shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
in Experiment 1.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)
Diflufenzopyr


timing


0.43


0.84


1.68


0.14


0.28


0.56


Grams/pot
Absent 0.5 0.2 0.6 0.4 0.8 0.2 0.8 0.2 1.0 + 0.6 0.7 0.2
3 days prior 0.5 0.0 1.0 + 0.2 0.9 0.0 0.9 + 0.4 0.9 0.4 0.6 + 0.4
Tank-mix 0.7 0.2 0.8 0.2 0.6 0.2 0.5 0.1 0.4 0.2 0.7 0.2
3 days after 0.7 0.2 1.2 0.2 1.2 0.2 1.0 + 0.4 0.9 0.2 0.7 0.2
.Means followed by 95% confidence interval.

Table 3-4. Torpedograss rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
in Experiment 1.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)
Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56
Grams/pot
Absent 2.5 + 0.0 4.4 0.6 4.2 0.6 5.3 + 2.2 1.0 + 0.6 4.5 + 1.0
3 days prior 4.5 0.8 6.5 + 2.4 0.9 0.0 5.3 + 2.0 4.5 0.8 4.0 + 1.4
Tank-mix 3.5 + 0.6 5.1 + 3.6 2.8 0.8 2.3 0.4 3.8 + 2.2 2.5 0.6
3 days after 6.3 1.6 6.4 1.6 9.3 3.0 6.3 4.8 4.1 + 1.2 3.0 1.6
.Means followed by 95% confidence interval.









Table 3-5. Overall model variance for the visual evaluation, shoot regrowth biomass, and
rhizome biomass 8 weeks after initial treatment in the torpedograss diflufenzopyr
timing Experiment 2.
Visual evaluation Shoot regrowth Rhizome
Variables p-value p-value p-value
Experiment1 < 0.0001 < 0.0001 < 0.0001
Timing 0.5319 0.6704 0.3534
Herbicide 0.2795 0.6669 0.2225
Timing*herbicide 0.5828 0.2604 0.4043
Herbicide rate 0.0190 0.0817 0.2778
Timing*rate 0.5427 0.4561 0.4010
Herbicide*herbicide rate 0.5720 0.2876 0.1203
Timing*herbicide*herbicide rate 0.1708 0.6870 0.2002
Rep 0.5383 0.5026 0.1541
.Experiment comparison between experiment 1 and experiment 2 for the torpedograss
diflufenzopyr study.

Table 3-6. Percent control of torpedograss regrowth 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
in Experiment 2.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)
Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56
% Control
Absent 15 6 38 30 33 10 25 26 28 22 23 26
3 days prior 40 + 8 23 16 15 12 20 24 43 30 48 36
Tank-mix 18 24 50 34 23 10 15 6 55 34 23 32
3 days after 18 10 35 20 33 22 28 22 38 10 23 20
.Means followed by 95% confidence interval.

Table 3-7. Torpedograss shoot regrowth (grams/pot) 8 weeks after treatment by multiple rates of
glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings in
Experiment 2.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)
Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56
Grams/pot
Absent 0.9 0.2 0.6 0.4 0.6 0.2 1.2 1.0 0.9 1.0 0.9 0.6
3 days prior 0.4 0.0 0.8 0.4 1.1 0.4 1.0 + 0.6 0.7 0.6 0.4 0.6
Tank-mix 1.2 0.6 0.4 0.2 0.8 0.6 0.9 0.2 0.4 0.6 0.2 0.2
3 days after 0.8 0.6 0.6 0.4 1.0 1.0 0.7 0.8 0.4 0.2 0.7 0.6
.Means followed by 95% confidence interval.









Table 3-8. Torpedograss rhizome biomass (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by diflufenzopyr applied at 3 timings
in Experiment 2.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)
Diflufenzopyr timing 0.43 0.84 1.68 0.14 0.28 0.56
Grams/pot
Absent 5.5 0.6 4.2 2.6 4.0 1.0 5.2 2.8 5.7 2.0 4.7 0.6
3 days prior 2.1 0.8 4.6 2.6 5.9 2.2 6.1 5.2 6.2 5.2 2.5 2.0
Tank-mix 6.3 2.8 1.7 1.2 3.0 1.8 4.3 2.8 4.2 3.2 2.3 1.2
3 days after 4.5 3.0 3.5 2.4 6.0 4.8 5.0 5.0 1.7 0.4 2.5 1.4
.Means followed by 95% confidence interval.

Table 3-9. Overall model variance for the visual evaluation, shoot regrowth biomass, and
rhizome biomass 8 weeks after initial treatment in the torpedograss growth regulator
Experiment 1.
Visual evaluation Shoot regrowth Rhizome
Variables p-value p-value p-value
Experiment1 0.0002 < 0.0001 < 0.0001
Growth regulator 0.0210 0.0578 0.2589
Herbicide 0.0714 0.2558 0.0589
Growth regulator*herbicide 0.0638 0.8696 0.7799
Herbicide rate 0.3293 0.0578 0.0589
Growth regulator*herbicide rate 0.0171 0.0132 0.3582
Herbicide*herbicide rate 0.7065 0.1877 0.0523
Growth regulator *herbicide*herbicide rate 0.0255 0.0007 0.0691
Rep 0.6966 0.5949 0.0948
.Experiment comparison between experiment 1 and experiment 2 for the torpedograss growth
regulator study.

Table 3-10. Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in
Experiment 1.
Glyphosate (kg-ai/ha)1 Imazapyr (kg-ai/ha)
Growth Control. 0.43 0.84 1.68 0.14 0.28 0.56
regulator
% Control
Absent 0 +02 25 10 38 38 25 26 33 18 20 8 28 6
2,4-D 15 12 25 6 35 32 25 12 13 12 45 22 75 10
Dicamba 35 36 18 18 8 6 35 12 22 8 17 6 33 12
Quinclorac 18 12 25 12 8 10 20 + 8 30 14 25 18 8 10
Triclopyr 30 12 28 12 35 10 28 20 38 26 28 32 33 16
1Growth regulating herbicides applied alone or in the absence of glyphosate or imazapyr. 2Means
followed by 95% confidence interval.









Table 3-11. Torpedograss shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in
Experiment 1.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)
Growth
regulator Control. 0.43 0.84 1.68 0.14 0.28 0.56
Grams/pot
Absent 0.8 0.42 1.1 0.2 1.3 1.4 1.2 0.6 0.6 0.2 1.2 0.4 1.3 0.8
2,4-D 1.3 0.2 1.0 + 0.4 1.2 0.8 1.3 0.6 2.2 1.0 0.8 0.6 0.3 0.4
Dicamba 1.0 + 0.8 1.6 0.4 2.2 0.6 0.9 0.2 1.0 + 0.2 1.3 0.6 0.9 0.4
Quinclorac 1.4 0.2 1.0 + 0.4 2.5 1.0 1.0 + 0.2 1.1 0.8 1.4 0.6 1.8 0.4
Triclopyr 1.1 0.4 1.0 + 0.4 0.9 0.2 1.3 1.0 0.9 0.6 1.3 0.8 0.8 0.2
.Growth regulating herbicides applied alone or in the absence of glyphosate or imazapyr. 2Means
followed by 95% confidence interval.

Table 3-12. Torpedograss rhizome biomass (grams/pot) 8 weeks after initial treatment by
multiple rates of glyphosate or imazapyr, as influenced by growth regulating
herbicides in Experiment 1.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)


Growth
regulator


Control1 0.43


0.84


1.68


0.14


0.28


0.56


Grams/pot
Absent 6.7 2.62 8.1 2.4 7.7 8.2 2.6 0.4 5.2 3.6 7.3 3.2 6.4 3.2
2,4-D 9.1 2.6 6.8 1.4 5.8 3.2 4.8 1.0. 10.0 3.2 7.9 4.4 4.5 1.2
Dicamba 6.7 4.2 8.4 2.0 8.8 0.4 3.2 1.0 6.7 26 7.7 2.0 5.4 2.0
Quinclorac 8.9 5.4 6.0 1.8 9.7 3.8 3.2 4.0 5.2 1.0 7.3 1.6 9.2 1.8
Triclopyr 7.9 2.8 5.9 3.0 5.2 0.8 4.8 2.0 3.6 1.0 7.2 3.6 4.0 1.4
.Growth regulating herbicides applied alone or in the absence of glyphosate or imazapyr. 2Means
followed by 95% confidence interval.









Table 3-13. Overall model variance for the visual evaluation, shoot regrowth biomass, and
rhizome biomass 8 weeks after initial treatment in the torpedograss growth regulator
Experiment 2.


Visual evaluation Shoot regrowth
p-value p-value


Variables


Rhizome
p-value


Experiment1 0.0002 < 0.0001 < 0.0001
Growth regulator 0.0036 0.1444 0.4510
Herbicide 0.4440 0.9845 0.4730
Growth regulator*herbicide 0.7152 0.8329 0.5798
Herbicide rate 0.2019 0.5166 0.3138
Growth regulator*herbicide rate 0.0168 0.2622 0.4209
Herbicide*herbicide rate 0.1257 0.3600 0.5778
Growth regulator *herbicide*herbicide rate 0.5232 0.2622 0.8764
Rep 0.9979 0.5362 0.6994
.Experiment comparison between experiment 1 and experiment 2 for the torpedograss growth
regulator study.

Table 3-14. Percent control of cogongrass regrowth 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in
Experiment 2.


Glyphosate (kg-ai/ha)'


Imazapyr (kg-ai/ha)


Growth
regulator Control. 0.43 0.84 1.68 0.14 0.28 0.56
% Control
Absent 18 222 20 16 33 12 18 10 20 8 43 18 28 18
2,4-D 43 24 50 14 23 10 33 6 67 30 28 12 23 10
Dicamba 33 26 73 26 33 10 45 26 45 26 53 20 48 18
Quinclorac 20 + 18 35 34 28 24 50 36 20 12 25 6 33 22
Triclopyr 35 26 35 18 15 12 50 24 38 30 40 8 35 20
.Growth regulating herbicides applied alone or in the absence of glyphosate or imazapyr. 2Means
followed by 95% confidence interval.









Table 3-15. Torpedograss shoot regrowth (grams/pot) 8 weeks after initial treatment by multiple
rates of glyphosate or imazapyr, as influenced by growth regulating herbicides in
Experiment 2.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)
Growth
regulator Control1 0.43 0.84 1.68 0.14 0.28 0.56
Grams/pot
Absent 0.6 0.4.1 0.9 0.4 0.9 0.6 0.9 0.4 1.3 0.8 0.6 0.4 1.1 0.6
2,4-D 0.6 0.4 0.4 0.4. 1.1 0.8 0.6 0.2 0.6 0.6 0.9 0.6 0.9 0.2
Dicamba 0.5 0.4 0.2 0.4 0.8 0.6 0.6 0.6 0.5 0.4 0.4 0.2 0.4 0.2
Quinclorac 1.2 0.8 1.1 0.8 0.7 0.4 0.7 1.2 0.7 0.2 0.8 0.4 0.6 0.4
Triclopyr 0.8 0.6 1.1 0.8 0.7 0.2 0.4 0.4 1.4 1.6 0.6 0.2 0.5 0.2
.Growth regulating herbicides applied alone or in the absence of glyphosate or imazapyr. 2Means
followed by 95% confidence interval.

Table 3-16. Torpedograss rhizome biomass (grams/pot) 8 weeks after initial treatment by
multiple rates of glyphosate or imazapyr, as influenced by growth regulating
herbicides in Experiment 2.
Glyphosate (kg-ai/ha) Imazapyr (kg-ai/ha)
Growth
regulator Control. 0.43 0.84 1.68 0.14 0.28 0.56
Grams/pot
Absent 3.7 3.22 5.4 3.6 5.0 2.4 3.8 1.4 6.2 4.0 4.0 2.6 8.2 7.6
2,4-D 3.8 2.0 5.3 3.4 7.5 6.0 2.2 1.4 2.8 3.6 4.3 2.4 3.3 3.0
Dicamba 6.8 5.4 1.2 1.2 3.7 1.8 2.6 2.6 3.1 2.4 4.3 1.4 1.9 0.8
Quinclorac 5.0 3.2 4.4 2.8 4.2 2.2 3.1 2.2 3.5 1.4 4.2 2.6 3.8 1.8
Triclopyr 7.1 6.6 5.0 2.6 3.8 + 1.8 1.6 + 1.0 12.1 + 19.8 4.7 + 3.6 3.4 + 1.8
.Growth regulating herbicides applied alone or in the absence of glyphosate or imazapyr. 2Means
followed by 95% confidence interval.









CHAPTER 4
EVALUATION OF GROWTH REGULATOR HERBICIDES FOR IMPROVED CONTROL
OF COGONGRASS

Introduction

The state of Florida has been a world leader in the phosphate mine industry since the early

1900s (El-Midany 2004, FIPR 2004a). Extensive mining leads to 4,000 to 6,000 acres of

disturbed land annually, which is often exploited by invasive species, such as cogongrass

[Imperata cylindrica (L.) Beauv.] (FIPR 2004b, Ewel 1986).

Cogongrass, an invasive perennial grass, appears on multiple state noxious weed lists, as

well as the federal list (Dickens 1974, Holm et al. 1977, USDA 2005a, 2005b). One of the major

reasons that cogongrass is such a successful invader is due to its extensive rhizome system.

These rhizomes comprise greater than 60% of the entire plant's biomass (Sajise 1976). Eussen

(1979) reported eleven weeks after initial rhizome growth, the rhizome mass may occupy an area

as large as 4m2. In a mature stand, cogongrass can develop as many as 350 shoots from its

rhizome mass in a 6-week period (Eussen 1979).Terry et al. (1997) suggested that cogongrass

may even sacrifice leaf production to maintain a healthy rhizome base.

Complete control of cogongrass requires total removal of all viable tillers and rhizomes

(Tanner et al. 1992, Willard et al. 1997). The current best management practices for cogongrass,

regardless of method or integration of methods, cannot effectively control the plant to the point

of complete eradication without tremendous and often unfeasible means (Willard et al. 1997).

A number of herbicidal studies have been performed on cogongrass (Dickens and

Buchanan 1975). Herbicide applications to cogongrass are often difficult due to the high level of

rhizomes compared to leaves present (Coile and Shilling 1993). Those herbicides that have

provided the best results with the fewest adverse effects include glyphosate [N-

(phosphonomethyl) glycine], imazapyr (2-[4,5-dihydro-4-methyl-4-(1-methylethyl)-5-oxo-l-H-









imidazol-2-yl]-3-pyridinecarboxylic acid), and dalapon (2,2-Dichloropropionic acid, no longer

registered) (Willard et al. 1997).

Willard et al. (1996) reported that glyphosate and imazapyr can control cogongrass better

than dalapon in the absence of mechanical treatments. Glyphosate produces rapid cogongrass

defoliation, with no soil residual activity (Townsend and Butler 1990). Imazapyr is slower

acting, but residual soil activity (25 to 142 day half life) provides better long term control

(Johnson et al. 1997, Willard et al. 1997, WSSA 2002).

Applications of 3.4 kg-ai/ha of glyphosate or 0.8 kg-ai/ha of imazapyr provided 60 and

70% cogongrass control, respectively. However, when these herbicides were sequentially

applied, control ranged from 87 to 98% control 19 months after initial treatment regardless of

application order (Willard et al. 1997). There have been several reports that glyphosate or

imazapyr herbicide applications in the fall provide increased control (Gaffney 1996, Johnson et

al. 1999). Gaffney (1996) also indicated > 20% more control was achieved 1 year after treatment

with the same herbicides and rates in a fall application versus a spring or summer application.

Although seed spread is a concern, the biggest hurdle in developing a viable management

strategy for cogongrass is control of rhizomes. Rhizomes exhibit apical dominance which

suppresses the growth of shoots from subapical nodes (Cline 1994). Studies with auxinic

hormones suggest that auxins play a role in apical dominance in cogongrass, possibly causing

unequal distribution of carbohydrates and, consequently, systemic herbicides in the rhizomes

(Gaffney and Shilling 1995, Gaffney 1996). Gaffney (1996) reported that cogongrass rhizomes

with apices removed produced 31% more shoots than rhizomes with intact apices. Therefore,

disruption of normal auxin levels in rhizome grasses may release stored carbohydrates and

encourage new shoot production of otherwise dormant buds (Cline 1994, English 1998). This









generally occurs with physical injury, but it has been hypothesized that growth regulator

herbicides could cause this effect as well. By disrupting apical dominance, systemic herbicides

may be distributed more evenly and potentially provide more complete control.

Herbicides in the growth regulator classification interfere with growth hormone functions

and have similar modes of action and selectivity (Anderson 1996). Although the true mode of

action for many of these herbicides is unknown, it is speculated some have auxin-like properties

that mimic auxins in an unregulated fashion within plant tissues (Anderson 1996, Lym and

Deibert 2005). Other growth regulating herbicides such as diflufenzopyr inhibit the transport of

auxins (Grossman et al. 2002, WSSA 2002).

Limited information is available on the use of PGR herbicides such as triclopyr, dicamba,

2,4-D, and diflufenzopyr and quinclorac for cogongrass control. Preliminary studies suggest that

certain PGR herbicides, specifically 2,4-D and diflufenzopyr (1.12 and 0.28 kg-ai/ha

respectively) when tank-mixed with imazapyr (0.56 kg-ai/ha) may provide acceptable control of

regrowth (> 85%) for at least 8 weeks after initial treatment (WAIT) (Ketterer et al. 2006,

Ketterer et al. 2007). These results, although informative, do not clarify how well these

treatments will work in the field. If apical dominance can be disrupted using these PGR

herbicides and thus stimulate shoot growth, then perhaps an initial application of PGR herbicides

followed by a glyphosate or imazapyr treatment would provide better herbicide efficacy. The

objective of this study was to evaluate the effect of several growth regulating herbicides for

improved efficacy of glyphosate and imazapyr for cogongrass control. Pre-treatment interval and

time of year were also evaluated within the context of this objective. This timing component was

included in this study to evaluate whether a pre-conditioning period is needed (to stimulate

axillary bud break and sprouting).









Materials and Methods


Methodology

Field studies were conducted at Tenoroc Fish Management Area in Polk County, Florida.

This site was originally a phosphate mine, but is currently infested with dense and mature stands

of cogongrass. The entire area was burned in February of 2006. Studies were initiated in spring

(March) 2006, and herbicide treatments were applied 3 times throughout the year; experiment 1

spring (March), experiment 2 summer (June), experiment 3 fall (September).

All herbicides were applied using a CO.2. pressurized sprayer calibrated to deliver 187 L/ha.

A non-ionic surfactant (0.25% v/v) was added with each herbicide. Plant growth regulating

herbicide treatments included diflufenzopyr (0.28 kg-ai/ha), triclopyr (0.42 kg-ai/ha), quinclorac

(1.40 kg-ai/ha), dicamba (0.56 kg-ai/ha) and 2,4-D (1.12 kg-ai/ha). Within each growth regulator

herbicide treatment, imazapyr (0.84 kg-ai/ha) or glyphosate (3.36 kg-ai/ha) herbicides were

applied one time at 4 timing intervals. These intervals included 0 (same day), 1, 2, or 3 months

after the initial PGR herbicide treatment. The experiment was a split plot design, with the main

effect being PGR herbicide treatment and herbicide and application timing being subplot effects.

Visual evaluations were taken 3, 6, and 9 months after the initial PGR herbicide application and

based on the following scale: 0 = no control; 100 = complete control.

Statistical Analysis

The data were analyzed using proc GLM program in SAS 9.1. Treatments were regarded

as split-plot occurring within growth regulating herbicide. Models for the independent variables

(experiment, growth regulator, herbicide, and month of application) were determined using the

dependent variables (3, 6, and 9 month evaluations). Means and least significant difference

(LSD) were determined for the dependent variables according to the growth regulator, the

herbicide, and the month of herbicide application.









Results


Spring Experiment

Three month evaluation. There was a significant (p < 0.05) two-way interaction with

herbicide and month (Table 4-1). Averaged across all PGR herbicides, glyphosate and imazapyr

treatments did not differ within month of herbicide application for the 3 month evaluation after

the initial PGR herbicide treatments (Table 4-2). When glyphosate was applied 3 months after

the initial PGR herbicides, less control was observed compared to the remaining herbicide

application months. Imazapyr applied on the same day (0 month) as the PGR herbicides provided

more control compared to when it was applied 2 or 3 months after.

There was a significant (p < 0.05) two-way interaction with month and growth regulating

herbicide (Table 4-1). When treatments were applied on the same day (0 month) as the PGR

herbicides, 2,4-D provided the least control, when averaged across herbicide (Table 4-3).

Dicamba with glyphosate or imazapyr at the 0 month application provided 84% control, but did

not differ from quinclorac or triclopyr treatments. When glyphosate or imazapyr were applied 1

month after the initial PGR herbicides dicamba, diflufenzopyr, and triclopyr treatments provided

the most control. Varying levels of control were observed when glyphosate or imazapyr were

applied 2 months after the PGR herbicides, and no treatment exceeded 60% control. When

glyphosate or imazapyr were applied 3 months after any PGR herbicides < 35% control was

observed.

Six month evaluation. There was a significant (p < 0.05) two-way interaction with

herbicide and month (Table 4-1). Averaged across PGR herbicides, control within glyphosate for

the 6 month evaluation in the spring experiment was lower for the 0 month herbicide timing

(same day application) compared to when glyphosate was applied 2 or 3 months after the PGR

herbicides (Table 4-4). Glyphosate control did not exceed 65% when it was applied the same day









as (0 month) or 1 month after the initial PGR herbicide treatment. Imazapyr treatments did not

differ across months, providing > 94% control.

There was a significant (p < 0.05) two-way interaction with herbicide and growth regulator

(Table 4-1). Imazapyr control was greater when mixed with 2,4-D, diflufenzopyr, and

quinclorac, compared to glyphosate, when averaged across month of application. (Table 4-5).

Glyphosate control with dicamba or triclopyr was greater in comparison to 2,4-D but did not

differ from the remaining PGR herbicides. Imazapyr treatments provided > 93% control with any

PGR herbicide.

There was a significant (p < 0.05) two-way interaction with month and growth regulating

herbicide (Table 4-1). Averaged across herbicides, when glyphosate or imazapyr was applied 2

or 3 months after the initial PGR herbicides, > 80% control was observed with any PGR

herbicide. (Table 4-6). Control was greatest with 2,4-D when glyphosate or imazapyr were

applied 1, 2, and 3 months after 2,4-D. When glyphosate or imazapyr were applied 0, 1, or 2

months after dicamba, the level of control was higher compare to when glyphosate or imazapyr

was applied 3 months after dicamba. Control was greatest for diflufenzopyr, quinclorac, and

triclopyr when glyphosate or imazapyr were applied 2 or 3 months after.

Nine month evaluation. There was a significant (p < 0.05) two-way interaction with

herbicide and month (Table 4-1). Across all PGR herbicides, imazapyr provided more control

than glyphosate when applied 0, 1, and 2 months after PGR herbicides for the 9 month

evaluation on the spring experiment (Table 4-7). However, no difference was observed when

these herbicides were applied 3 months after the initial PGR herbicides. When glyphosate was

applied 2 and 3 months after the PGR herbicides, control was greater compared to the same day









(0 month) treatment. Imazapyr provided > 89% control when applied at any month of

application.

There was a significant (p < 0.05) two-way interaction with herbicide by growth regulator

(Table 4-1). Averaged across herbicide application months, imazapyr provided more control with

2,4-D compared to glyphosate (Table 4-9). The remainder of the glyphosate/imazapyr treatments

did not differ within PGR herbicides. Dicamba and triclopyr provided more control compared to

2,4-D or diflufenzopyr, when mixed with glyphosate. Imazapyr treatments provided > 86%

control with any PGR herbicide.

There was a significant (p < 0.05) two-way interaction with month and growth regulating

herbicide (Table 4-1). Averaged across glyphosate/imazapyr treatments, the best control was

observed when glyphosate or imazapyr were applied 2 and 3 months after 2,4-D, dicamba, and

triclopyr (Table 4-9). However, dicamba treatments did not differ across month of herbicide

application. When glyphosate or imazapyr was applied 3 months after diflufenzopyr, control was

greater compared to the remaining herbicide application months. Quinclorac provided the most

control when glyphosate or imazapyr was applied 2 months after, compared to the remaining

application months.

Summer Experiment

Three month evaluation. There was no significant (p < 0.05) interaction (Table 4-1).

However, the variables month and growth regulator were significant, while herbicide was not.

Averaged across glyphosate or imazapyr and month of herbicide application, the greatest control

was observed with 2,4-D, dicamba, and diflufenzopyr for the 3 month evaluation on the summer

experiment (Table 4-11). However, diflufenzopyr did not differ from the remaining PGR

herbicides treatments. Averaged across PGR herbicides and glyphosate or imazapyr, when









herbicides were applied on the same day (0 month) as the PGR herbicides > 92% was observed

(Table 4-12). The 3 month herbicide application provided almost no control.

Six month evaluation. There was a significant (p < 0.05) two-way interaction with

herbicide and month, but no three-way interaction (Table 4-10). Across PGR herbicides,

imazapyr provided more control when applied on the same day (0 month) as the PGR herbicide,

for the 6 month evaluation on the summer experiment compared to glyphosate (Table 4-13).

However, glyphosate yielded more control when applied 3 months after PGR herbicide. This

glyphosate treatment provided greater control than when applied at the 0 or 1 month application.

When imazapyr was applied 0, 1, or 2 months after the initial PGR herbicides control was >

89%.

Growth regulator was a significant (p < 0.05) variable (Table 4-10). Greater than 75%

control was observed for all of the PGR herbicide treatments (Table 4-14). Dicamba and 2,4-D

provided greater control compared to quinclorac or triclopyr.

Fall Experiment

Three month evaluation. There was no significant (p < 0.05) interaction (Table 4-15).

However, the variables month and growth regulator were significant when examined alone

(Table 4-15). The PGR herbicide treatments, averaged across herbicide and month of herbicide

application, failed to provide > 70% control in the 3 month evaluation on the fall experiment

(Table 4-16). Dicamba, and 2,4-D provided the greatest level of control compared to the

remaining PGR herbicides. When averaged across glyphosate or imazapyr and PGR herbicides,

the 0 and 1 month herbicide application timing provided greater control compared to the 2 and 3

month herbicide application (Table 4-17). When glyphosate or imazapyr applications occurred 2

and 3 months after the initial PGR herbicide application, control was < 50%.









Discussion

Acceptable cogongrass control is defined as having > 80% reduction in rhizome biomass 2

years after treatment (Willard et al. 1996). This level of control can best be achieved if the

management method targets the rhizomes and all viable tillers (Tanner et al. 1992, Willard et al.

1997). In this experiment, the rhizomes were targeted using growth regulator herbicides and

either glyphosate or imazapyr. However, rhizome data were not examined and acceptable

control, in this study, is defined as > 80% injury or visual reduction, 3, 6, or 9 months after initial

treatment (MAT).

The evaluation 3 months after initial treatment (MAT) did not accurately reflect data

trends. Glyphosate or imazapyr treatments applied 3 months after the initial PGR herbicides

occurred just minutes before the evaluation. Thus, results may appear biased in reflecting that the

0 month (same day application as the PGR herbicides) treatments provided more control

compared to the 3 month application when evaluated 3 MAT, when, in fact, the 0 month

treatments were allowed the necessary interval between application and injury symptoms. The

interval was not long enough to observe these symptoms when glyphosate or imazapyr were

applied 3 months after PGR herbicides.

There does appear to be a critical time frame between application of any PGR herbicide

followed by either glyphosate or imazapyr. If the PGR herbicides are applied first and imazapyr

application follows either the same day (0 month) or 1 or 2 months after, cogongrass control can

be > 89% starting at 6 MAT and continuing through 9 MAT. For glyphosate, > 80% control at 6

and 9 MAT occurred when the herbicide was applied 2 or 3 month after the PGR herbicides.

Another trend was the consistent control observed with imazapyr and any PGR herbicide,

> 85% at 6 and 9 months. Studies by Ketterer et al. (2006 and 2007) indicated that one would

expect similar results on cogongrass with 2,4-D or diflufenzopyr and imazapyr in the









greenhouse. The most consistent control with glyphosate occurred with triclopyr and dicamba

treatments, approximately 85% control for triclopyr and approximately 80% control with

dicamba 6 and 9 MAT. These findings compliment observations by Flint and Barrett (1989). A

study on johnsongrass (Sorghum halepense L.) indicated that glyphosate and dicamba (0.28,

0.49, and 0.56 kg-ai/ha) had antagonistic effects on shoot production at low rates of glyphosate,

0.28 and 0.56 kg-ai/ha. The chemicals then became synergistic when glyphosate rates increased

above 0.56 kg-ai/ha (Flint and Barrett 1989). Triclopyr has been documented to have synergistic

effects with other herbicides such as clopyralid (Bovey and Whisenat 1992). However, no such

documentation occurs on the synergism of triclopyr and glyphosate.

This study was replicated in the spring, summer, and fall. Previous studies indicate that

herbicide applications in the fall tend to result in greater efficacy compared to spring treatments

(> 20% more control, 12 months after treatment) for both glyphosate and imazapyr as they are

actively translocated with the photosynthates to the rhizomes (Tanner et al. 1992, Gaffney 1996,

Johnson et al. 1997). It can be expected that glyphosate (2.24 kg-ai/ha) or imazapyr (0.84 kg-

ai/ha) treatments on cogongrass will provide approximately 70-80% control up to 1 year after

treatment when applied in the fall. Similar levels of control were observed 9 MAT for the spring

study. The inclusion of PGR herbicides with glyphosate or imazapyr treatment could result in

more complete control regardless of the season.

Although the results appear promising for cogongrass control, the issue of long-term

control has yet to be established as the data presented are only indicative of 9 month ratings after

only the spring treatment. The majority of experimental plots with 100% control were either bare

ground or covered by volunteer weeds such as hairy indigo (Indigofera hirsuta L.) and passion

flower (Passiflora incarnate L.). Bare ground plots are a cause for concern if the below-ground









rhizomes still prove viable or cogongrass seeds are present in the seed-bank. Burke and Grime

(1996) found that open niches such as bare ground correlate with an influx of invasive species.

However, high densities of volunteer weeds may help suppress cogongrass development. For

example, landholders are encouraged to use legumes such as velvetbean (Mucunapruriens var.

utilis) in areas where cogongrass is problematic (Akobundu et al. 2000, Versteeg and

Koudokpon 1990). Leguminous cover crops seem to be the most effective competitor to

cogongrass due to nitrogen fixation and soil enhancement from the plant (Ibewiro et al. 2000).

The problem with cultural control is that some cover species may require 2-5 years to become

effective in slowing or reducing cogongrass (Akobundu et al. 2000). However, in this study,

cover species were not directly planted after treatment. Natural seed banks within the soil

contributed the volunteer species which were able to recover and shade out cogongrass within 3-

6 months. Although there is no supporting data, it has been suggested that the leguminous hairy

indigo may be imazapyr resistant (Conway Duever 2003) and shows promise of future control as

legumes have been recommended as cover crops (Ibewiro et al. 2000).

Table 4-1. Overall model variance for the control evaluations 3, 6, and 9 months after treatment
(MAT) in the cogongrass spring field experiment.
Variables 3 MAT 6 MAT 9 MAT
Rep 0.0016 0.5394 0.7280
Herbicide 0.0310 < 0.0001 < 0.0001
Month < 0.0001 < 0.0001 < 0.0001
Herbicide*month 0.0073 < 0.0001 < 0.0001
Growth regulator 0.0018 0.0102 0.0089
Herbicide*growth regulator 0.1213 0.0047 0.0215
Month*growth regulator 0.0388 0.0093 0.0186
Herbicide*month*growth regulator 0.4524 0.5393 0.1778









Table 4-2. Averaged across plant growth regulating herbicides, the effect of herbicide and month
of application on cogongrass control 3 months after initial plant growth regulating
herbicide application for the spring experiment.
Month of herbicide application1
0 1 2 3
% Control
Glyphosate 63*a 65*a 51*a 30*b
Imazapyr 80*a 67*ab 54*b 25*c
1Means within month (column) followed by the same symbol are not significantly different
LSD (0.05) = 19. Means within herbicide (row) followed by the same letter are not significantly
different LSD (0.05) = 15.

Table 4-3. Averaged across herbicides, the effect of plant growth regulating herbicide and month
of application on cogongrass control 3 months after initial plant growth regulating
herbicide application for the spring experiment.
Month1 2,4-D2 Dicamba Diflufenzopyr Quinclorac Triclopyr
% Control
0 53*c 84*a 69*b 76*ab 76*ab
1 58*b 76*a 69*a 56tb 70*a
2 48*bc 56tab 60*a 53tab 45tbc
3 25ta 24ma 29ta 28ma 33fa
.Month of glyphosate or imazapyr application. 2Means within growth regulator (column)
followed by the same symbol are not significantly different LSD (0.05) = 17. Means within
month (row) followed by the same letter are not significantly different LSD (0.05) = 9.

Table 4-4. Averaged across plant growth regulating herbicides, the effect of herbicide and month
of application on cogongrass control 6 months after initial plant growth regulating
herbicide application for the spring experiment.
Month of herbicide application1
0 1 2 3
% Control
Glyphosate 51fb 62*ab 87*a 87*a
Imazapyr 99*a 95*a 100*a 94*a
1Means within month (column) followed by the same symbol are not significantly different LSD
(0.05) = 38. Means within herbicide (row) followed by the same letter are not significantly
different LSD (0.05) = 30









Table 4-5. Averaged across month of application, the effect of herbicide and growth regulator on
cogongrass control 6 months after initial plant growth regulating herbicide application
for the spring experiment.
2,4-D. Dicamba Diflufenzopyr Quinclorac Triclopyr
% Control
Glyphosate 57fb 86*a 71tab 60tab 82*a
Imazapyr 99*a 93*a 99*a 94*a 100*a
1Means within growth regulator (column) followed by the same symbol are not significantly
different LSD (0.05) = 26. Means within herbicide (row) followed by the same letter are not
significantly different LSD (0.05) = 24.

Table 4-6. Averaged across herbicide, the effect of growth regulator and month of application on
cogongrass control 6 months after initial plant growth regulating herbicide application
for the spring experiment.
Month1 2,4-D2 Dicamba Diflufenzopyr Quinclorac Triclopyr
% Control


0 51mb 94*a 71tb 70fb 86ta
1 80ta 89*a 81fa 55mb 85ta
2 91*a 94*a 93*a 96*a 98*a
3 95*a 81tb 95*a 86*ab 94*tab
iMonth of glyphosate or imazapyr application. 2Means within growth regulator (column)
followed by the same symbol are not significantly different LSD (0.05) = 10. Means within
month (row) followed by the same letter are not significantly different LSD (0.05) = 13.


Table 4-7. Averaged across plant growth regulating herbicide, the effect of growth regulator and
month of application on cogongrass control 9 months after initial plant growth
regulating herbicide application for the spring experiment.
Month of herbicide application1
0 1 2 3
% Control
Glyphosate 44tb 66tab 80ta 89*a
Imazapyr 97*a 95*a 100*a 89*a
.Means within month (column) followed by the same symbol are not significantly different LSD
(0.05) = 19. Means within herbicide (row) followed by the same letter are not significantly
different LSD (0.05) = 26.

Table 4-8. Averaged across month of application, the effect of growth regulator and herbicide on
cogongrass control 9 months after initial plant growth regulating herbicide application
for the spring experiment.
2,4-D1 Dicamba Diflufenzopyr Quinclorac Triclopyr
% Control


Glyphosate 59*b 84*a 59*b 64*ab 82*a
Imazapyr 98ta 94*a 98*a 86*a 100*a
1Means within growth regulator (column) followed by the same symbol are not significantly
different LSD (0.05) = 26. Means within herbicide (row) followed by the same letter are not
significantly different LSD (0.05) = 22.









Table 4-9. Averaged across herbicides, the effect of growth regulator and month of application
on cogongrass control 9 months after initial plant growth regulating herbicide
application for the spring experiment.
Month1 2,4-D. Dicamba Diflufenzopyr Quinclorac Triclopyr
% Control
0 50mc 91*a 59.bc 68tb 85ta
1 78ta 86*a 80tba 75ta 81fa
2 91*ab 93*a 79tb 91*ab 96*a
3 95*ab 85*b 96*ab 70tc 100*a
1Month of glyphosate or imazapyr application. 2Means within growth regulator (column)
followed by the same symbol are not significantly different LSD (0.05) = 10. Means within
month (row) followed by the same letter are not significantly different LSD (0.05) = 13.

Table 4-10. Overall model variance for the control evaluations 3 and 6 months after treatment
(MAT) in the cogongrass summer field experiment.
Variables 3 MAT 6 MAT
Rep 0.5204 0.1111
Herbicide 0.5133 0.1373
Month < 0.0001 0.4485
Herbicide*month 0.8638 < 0.0001
Growth regulator < 0.0001 0.0005
Herbicide*growth regulator 0.6661 0.6892
Month*growth regulator 0.8642 0.7400
Herbicide*month*growth regulator 0.9708 0.1678

Table 4-11. Effect of growth regulator, averaged across herbicide and month of glyphosate or
imazapyr application, on cogongrass control 3 months after initial plant growth
regulating herbicide application for the summer experiment.
Growth regulator1 % Control1
2,4-D 66a
Dicamba 63a
Diflufenzopyr 52ab
Quinclorac 47b
Triclopyr 47b
1Means followed by the same letter are not significantly different LSD (0.05) = 10.









Table 4-12. Effect of month of application, averaged across herbicide and plant growth
regulating herbicides, on cogongrass control 3 months after initial plant growth
regulating herbicide application for the summer experiment.
Month1. % Control.l
0 92a
1 70b
2 47c
3 lid
1Month of glyphosate or imazapyr application. 2Means followed by the same letter are not
significantly different LSD (0.05) = 7.

Table 4-13. Averaged across plant growth regulating herbicides, the effect of herbicide and
month of application on cogongrass control 6 months after initial plant growth
regulating herbicide application for the summer experiment.
Month of herbicide application1
0 1 2 3
% Control
Glyphosate 76fb 80*b 84*ab 93*a
Imazapyr 99*a 89*a 90*a 72fb
1Means within month (column) followed by the same symbol are not significantly different LSD
(0.05) = 12. Means within herbicide (row) followed by the same letter are not significantly
different LSD (0.05) = 10.

Table 4-14. Effect of growth regulator, averaged across herbicide and month of glyphosate or
imazapyr application, on cogongrass control 6 months after initial plant growth
regulating herbicide application for the summer experiment.
Growth regulator1 % Control1
2,4-D 93a
Dicamba 90a
Diflufenzopyr 87ab
Quinclorac 78b
Triclopyr 78b
1Means followed by the same letter are not significantly different LSD (0.05) = 9.

Table 4-15. Overall model variance for the control evaluation 3 months after treatment (MAT) in
the cogongrass fall field experiment.
Dependent variables 3 MAT
Rep 0.3062
Herbicide 0.3948
Month < 0.0001
Herbicide*month 0.4224
Growth regulator < 0.0001
Herbicide*growth regulator 0.4631
Month*growth regulator 0.6534
Herbicide*month*growth regulator 0.7867









Table 4-16. Effect of growth regulator, averaged across herbicide and month of glyphosate or
imazapyr application, on cogongrass control 3 months after initial plant growth
regulating herbicide application for the fall experiment.
Growth regulator1 % Control1
2,4-D 69a
Dicamba 68a
Diflufenzopyr 48b
Quinclorac 46b
Triclopyr 30b
.Means followed by the same letter are not significantly different LSD (0.05) = 14.

Table 4-17. Effect of month of application, averaged across herbicide and plant growth
regulating herbicide, on cogongrass control 3 months after initial plant growth
regulating herbicide application for the fall experiment.
Month.' % Control2
0 67a
1 62a
2 44b
3 34b
1Month of glyphosate or imazapyr application. .Means followed by the same letter are not
significantly different LSD (0.05) = 12.









CHAPTER 5
EVALUATION OF GROWTH REGULATOR HERBICIDES FOR IMPROVED CONTROL
OF TORPEDOGRASS

Introduction

Lake Okeechobee, the second largest closed-system freshwater lake in the United States

has a surface area of 1,732 km2 and an average depth of 2.7 meters (Jin et al. 1998). There are

roughly 40,000 ha of littoral zone in the lake; of which 6,000 ha of native plants have been

displaced by torpedograss (Panicum repens L.) (Schardt 1992). The presence of this plant

impacts the lake's multi-million dollar sport and recreation fisheries, as the monospecific stands

provide poor habitat for fish and water fowl (Hanlon and Langeland 2000). Torpedograss is a

serious detriment in Lake Okeechobee, as well as other aquatic systems in Florida and has been

ranked by the Florida Department of Environmental Protection as the 2nd most abundant plant in

Florida lakes since 1992 (Schardt 1992, Schardt personal communication, Feb 21, 2007). The

presence of torpedograss is additionally problematic in Florida because it interrupts flood

control, irrigation and turf production (Shilling and Haller 1989, McCarty et al. 1993).

Contributing to this threat are the plant's rhizomes. Torpedograss' large rhizome system

comprises 70 to 90% of the plant's biomass (Smith et al. 1999). When fragmented, rhizomes

buds can regenerate at a rate of 92 to 96% in temperatures of 20 to 35C (Hossain et al. 2001).

New buds are continuously produced along the entire length of the rhizomes indicating weak

apical dominance (Wilcut et al. 1988a). Since all of the nodes found on the rhizome system can

be viable, complete control of torpedograss requires total removal of all viable tillers and

rhizomes (Sutton 1996, Smith et al. 1999).

Most management studies on torpedograss come with mixed success, but few have

provided 100% long term control (> 12 months) within time constraints and budgets for the

average landowner (Manipura and Somaratne 1974, Willard et al. 1998, Smith et al. 1999).









Herbicidal studies have primarily focused on glyphosate and imazapyr (Baird et al. 1983,

Shilling and Haller 1989, Willard et al. 1998, Smith et al. 1999, Hanlon and Langeland 2000).

Limited control with these herbicides is often attributed to the aquatic habitat of torpedograss

where herbicide absorption occurs only on the emergent portion of the plant (Baird et al. 1983,

Smith et al. 1999). When using glyphosate only the emergent stems were controlled, but rapid

regrowth often occurred from rhizomes and submerged stem segments within a few months

(Baird et al. 1983). Smith et al. (1999) concluded that high water levels inhibit foliar interception

of glyphosate and control correlated with foliar exposure to water level ratio. To achieve > 90%

control (5 weeks after initial treatment), a glyphosate application rate of 2.24 kg-ai/ha was

needed to be intercepted by at least 40% of the foliage. Lower rates correlated with a higher

percentage of foliage cover to achieve similar results (Smith et al. 1999).

Imazapyr applications on torpedograss have similar problems with submergence, and in

turn, less control (Hanlon and Langeland 2000). Inconsistencies in data presented by Hanlon and

Langeland (2000) lead the authors to speculate that fluctuating water depth at different

experimental sites could have influenced results. While all experiments began in approximately

0.8m of water, by the end of the experiment, one study site was considered dry while the

remaining sites were flooded. Greater than 95% control was observed at the dry site with < 25%

control at the flooded sites. The authors also speculated that thatch levels may have contributed

to inconsistent control as the amount of torpedograss tissue exposed to the herbicide may be

reduced. This reduction may result from thatch blocking the herbicide from hitting the plants

(Hanlon and Langeland 2000).

While speculating that control with glyphosate or imazapyr is inversely proportional to

submerged tissue, considerations to improve herbicide efficacy arise. If torpedograss could be









stimulated to increase shoot production, allowing more of the plant to emerge, then herbicide

applications of glyphosate or imazapyr could potentially be more effective.

It was speculated that auxin-like herbicides could be used to stimulate shoot production.

Herbicides in this classification interfere with growth hormone functions and have similar modes

of action and selectivity (Anderson 1996). While the true mode of action of some of these

herbicides is unknown, it is speculated that some of these PGR herbicides mimic auxins and may

lead to increased sprouting at nodes (e.g. 2,4-D, dicamba, diflufenzopyr, quinclorac) (Anderson

1996, WSSA 2002, Lym and Deibert 2005). Other growth regulating herbicides such as

diflufenzopyr inhibit the transport of auxins (Grossman et al. 2002, WSSA 2002).

Limited information is available on the use of PGR herbicides such as triclopyr, dicamba,

2,4-D, and diflufenzopyr for torpedograss control. Previous greenhouse data suggest inconsistent

control was observed 8 weeks after initial treatment when PGR herbicides were combined with

either glyphosate or imazapyr (Ketterer et al. 2007). These results do not clarify how well these

treatments will work in the field. The objective of this study was to evaluate the effect of several

growth regulating herbicides in conjunction with glyphosate or imazapyr for torpedograss

control under field conditions.

Materials and Methods

Methodology

A field study was conducted on the north shore of Lake Okeechobee (270 05.985'N, 0800

55.680W) on a mature stand of densely populated torpedograss. In this site the torpedograss was

roughly 0.5 meters in height with a heavy thatch layer on the ground. The study was initiated in

May 2006. Treatments included 5 PGR herbicides (diflufenzopyr 0.28 kg-ai/ha, triclopyr 0.42

kg-ai/ha, quinclorac 1.4 kg-ai/ha, dicamba 0.56 kg-ai/ha, and 2,4-D 1.12 kg-ai/ha) tank-mixed

with either glyphosate (3.36 kg-ai/ha) or imazapyr (0.84 kg-ai/ha). Appropriate nonionic









surfactant volume (0.25% v/v) was applied with each treatment. Glyphosate and imazapyr were

applied without PGR herbicides for comparison along with an untreated control. All treatments

were applied using a backpack sprayer calibrated to deliver 187 L/ha. Efficacies of treatments

were visually evaluated as percent control based upon the growth and health of untreated plots (0

= no control, 100 = complete control) at 3, 6, and 9 months after treatment. The experiment was

arranged in a completely randomized block design with four replications.

Statistical Analysis

The data were analyzed using proc GLM program in SAS 9.1. The untreated control was

not included in the analyses to assess the impact of the growth regulating herbicides. Models for

the independent factors (growth regulator and herbicide) were determined using the dependent

variables (3, 6, and 9 month evaluations). Data were presented as means with 95% confidence

intervals

Results and Discussion

Analysis of variance indicated a significant (p < 0.05) two-way interaction with herbicide

and growth regulator for the evaluations 3, 6, and 9 months after treatment (MAT) (Table 5-1).

Plant growth regulating herbicides had no effect on glyphosate control 3, 6, or 9 MAT (Table 5-

2). Glyphosate control never exceeded 60%. Nine MAT, control from quinclorac with

glyphosate declined compared to 3 MAT.

Greater than 70% control was observed with imazapyr when applied alone or with

dicamba, diflufenzopyr, quinclorac, or triclopyr. With the exception of 2,4-D, the PGR

herbicides had no effect on the level of torpedograss control observed. Treatments with 2,4-D

provided almost no control throughout the experiment, indicating that the two herbicides

potentially nullified the effects of the other. Compared to the evaluation 3 MAT, control declined









for most PGR herbicides at 6 MAT. Treatments with diflufenzopyr declined 9 MAT compared to

3 MAT.

Possible explanations for the overall lack of control may be attributed to many things. The

torpedograss site was not flooded for the duration of the study, excluding theories by Smith et al.

(1999) who suggested glyphosate control of torpedograss was related to the proportion of

emergent stems to the intercepted herbicide rate. However, there was a thick layer of thatch

which Hanlon and Langeland (2000) suggested could possibly contribute to poor control with

imazapyr; this may also be a reason for the poor glyphosate control in this study. But

approximately 80% of the stem was above the thatch line and since glyphosate lacks soil activity

this should have no bearing on control. Imazapyr treatments yielded less than expected control,

in general. The residual activity of imazapyr tends to provide lengthy control due to its 25 to 142

day half-life in the soil (WSSA 2002). Poor torpedograss control was also observed with

glyphosate and imazapyr with PGR herbicides in greenhouse studies (Ketterer et al. 2007).

Therefore, it is possible that torpedograss simply did not respond to the PGR herbicide

treatments. Since long term control was not established with this study, further research is

warranted.

Table 5-1. Overall model variance for the control evaluations 3 and 6 months after treatment
(MAT) in the torpedograss field experiment.
Variable 3 MAT 6 MAT 9 MAT
Herbicide < 0.0001 < 0.0001 0.0004
Growth regulator < 0.0001 0.0022 0.1452
Herbicide*growth regulator < 0.0001 0.0045 0.0029
Rep 0.6192 0.3653 0.1355









Table 5-2. Influence of plant growth regulating herbicides applied with glyphosate and imazapyr
for control of torpedograss at 3, 6, and 9 months after treatment (MAT).
Glyphosate Imazapyr
Growth regulator 3 MAT 6 MAT 9 MAT 3 MAT 6 MAT 9 MAT
% Control
Absent 34 20.1. 30 14 20 12 73 42 65 34 63 20
2,4-D 50 14 40 24 38 26 0 0 8 6 5 6
Dicamba 53 10 48 28 28 28 93 6 73 10 43 22
Diflufenzopyr 53 10 53 24 43 28 90 + 8 80 + 8 55 18
Quinclorac 60 12 38 28 25 12 88 6 70 + 8 43 18
Triclopyr 45 26 30 14 13 18 93 6 65 20 63 12
.Means followed by 95% confidence interval.









CHAPTER 6
CONCLUSIONS

A study was derived to improve glyphosate and imazapyr efficacy using growth regulating

herbicides. The growth regulators chosen have auxin-regulating properties (Anderson 1996,

Cline 1997, Taiz and Zeiger 2006). By using these growth regulating herbicides to stimulate

shoot production, the goal was to provide more complete control by depleting the carbohydrate

reserves in the rhizomes as a result of shoot stimulation. It was hypothesized that the

combination of plant growth regulating (PGR) herbicides with glyphosate or imazapyr would

increase herbicide efficacy in cogongrass and torpedograss.

Both greenhouse and field studies were conducted using glyphosate and imazapyr

combined in various treatments with the PGR herbicides 2,4-D, dicamba, diflufenzopyr,

quinclorac, and triclopyr. Greenhouse treatments were separated into 2 studies. The first study

examined the effect of diflufenzopyr timing (0.22 kg-ai/ha). Either no diflufenzopyr was applied,

or it was applied either 3 days before, tank-mixed with, or 3 days after glyphosate or imazapyr

treatments. Glyphosate rates included 0.0, 0.43, 0.84, and 1.68 kg-ai/ha, while imazapyr rates

included 0.0, 0.14, 0.28, and 0.56 kg-ai/ha. The second study examined PGR herbicides (2,4-D

1.12 kg-ai/ha, dicamba 0.56 kg-ai/ha, triclopyr 0.56 kg-ai/ha, and quinclorac 1.40 kg-ai/ha) tank

mixed with either glyphosate or imazapyr with the previously mentioned rates. The field studies

examined whether shoot stimulation from PGR herbicides (2,4-D 1.12 kg-ai/ha, dicamba 0.56

kg-ai/ha, diflufenzopyr 0.28 kg-ai/ha, triclopyr 0.42 kg-ai/ha, and quinclorac 1.40 kg-ai/ha)

would result in better glyphosate or imazapyr efficacy (3.36 and 0.84 kg-ai/ha, respectively).

Torpedograss treatments were all tank-mixed and applied the same day, while glyphosate or

imazapyr treatments for cogongrass were applied once, on the same day (0 month) as PGR

herbicides or 1, 2, or 3 months after the initial PGR herbicide application.









Results from these experiments indicate that PGR herbicides provide varied levels of

control when used with glyphosate or imazapyr. In the greenhouse, consistent cogongrass control

came from imazapyr tank-mixed with diflufenzopyr or 2,4-D (> 80% control after 8 weeks with

0.56 kg-ai/ha of imazapyr). Torpedograss greenhouse results indicated no consistent trend in

control with and without the inclusion of PGR herbicides. In the field, cogongrass was best

controlled when imazapyr was applied with any PGR herbicide, for any tested intervals after

PGR herbicide application, approximately 85% or greater. When glyphosate was applied 2 or 3

months after PGR herbicides, greater than 80% control was observed after 6 and 9 months. Most

PGR herbicide treatments with torpedograss had no effect on glyphosate or imazapyr efficacy. It

appears that cogongrass control can be improved if treated with PGR herbicides. Thus, we can

conclude that we support our hypothesis for cogongrass. However, the advantage of

adding/combining PGR herbicides to glyphosate or imazapyr was not observed for torpedograss.









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BIOGRAPHICAL SKETCH

Born on September 29, 1982, Eileen is the second child of Martin and Margaret Ketterer.

She grew up in Altamonte Springs, Florida, with her mother and 2 brothers, Brian and Tommy,

where she attended Lyman High School. Her education continued at Bucknell University,

Lewisburg, Pennsylvania, where she received her Bachelor of Science with a concentration in

environmental studies. It was at Bucknell that she decided to venture into the world of weeds,

completing her senior thesis on purple loosestrife. Her education culminated at the University of

Florida, Gainesville, where she received a Master of Science with a concentration in agronomy,

specializing in weed science. Here she studied cogongrass and torpedograss as a requirement for

her master's thesis. Eileen plans to continue invasive weed eradication as well as increase public

awareness on the subject.