<b>HRAC Group 3</b> <font size='2'> (Legacy K1) </font> resistant Setaria viridis from United States, North Dakota

INTERNATIONAL HERBICIDE-RESISTANT WEED DATABASE

HRAC GROUP 3 (LEGACY K1) RESISTANT GREEN FOXTAIL
(Setaria viridis)

Inhibition of Microtubule AssemblyHRAC Group 3 (Legacy K1)

United States, North Dakota

INTRODUCTION		GREEN FOXTAIL
Green Foxtail (Setaria viridis) is a monocot weed in the Poaceae family. In North Dakota this weed first evolved resistance to Group 3 (Legacy K1) herbicides in 1989 and infests Sunflower, and Wheat. Group 3 (Legacy K1) herbicides are known as Inhibition of Microtubule Assembly (Inhibition of Microtubule Assembly ). Research has shown that these particular biotypes are resistant to trifluralin and they may be cross-resistant to other Group 3 (Legacy K1) herbicides. The 'Group' letters/numbers that you see throughout this web site refer to the classification of herbicides by their site of action. To see a full list of herbicides and HRAC herbicide classifications click here.

QUIK STATS (last updated Sep 15, 2000 )
Common Name	Green Foxtail
Species	Setaria viridis
Group	Inhibition of Microtubule Assembly HRAC Group 3 (Legacy K1)
Herbicides	trifluralin
Location	United States, North Dakota
Year	1989
Situation(s)	Sunflower, and Wheat
Contributors - (Alphabetically)	Mick Anderson, and Dallas Peterson
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NOTES ABOUT THIS BIOTYPE

AREAS FOUND

Dallas Peterson

Central North Dakota 13 counties.

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GENERAL

Dallas Peterson

Populations of resistant plants vary from low to 100% within affected area, occurence is predominant in monoculture wheat or where DNA's have been used every year in crop rotations.

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ACADEMIC ASPECTS

Confirmation Tests

Field, and Greenhouse trials comparing a known susceptible Green Foxtail biotype with this Green Foxtail biotype have been used to confirm resistance. For further information on the tests conducted please contact the local weed scientists that provided this information.

Genetics

Genetic studies on HRAC Group 3 resistant Green Foxtail have not been reported to the site. There may be a note below or an article discussing the genetics of this biotype in the Fact Sheets and Other Literature

Mechanism of Resistance

The mechanism of resistance for this biotype is either unknown or has not been entered in the database. If you know anything about the mechanism of resistance for this biotype then please update the database.

Relative Fitness

There is no record of differences in fitness or competitiveness of these resistant biotypes when compared to that of normal susceptible biotypes. If you have any information pertaining to the fitness of Group 3 (Legacy K1) resistant Green Foxtail from North Dakota please update the database.

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CONTRIBUTING WEED SCIENTISTS

MICK ANDERSON

Dow Agrosciences Ag. Chem, 6211 Saddle Creek Trl Fargo, 58104-6843, North Dakota United States

DALLAS PETERSON

Professor and Extension Weed Specialist Kansas State University Department of Agronomy 3703 Throckmorton Plant Sciences Center 1712 Claflin Road Manhattan, KS 66506-0110, Kansas United States Email Dallas Peterson Web : Web Site Link

ACKNOWLEDGEMENTS
The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in North Dakota have been instrumental in providing you this information. Particular thanks is given to Mick Anderson, and Dallas Peterson for providing detailed information.

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Herbicide Resistant Green Foxtail Globally
(Setaria viridis)

Country

FirstYear

Situation

Active Ingredients

Site of Action

Canada (Manitoba)

1988

Canola, Cropland, Spring Barley, and Wheat

ethalfluralin, and trifluralin

Inhibition of Microtubule Assembly ( HRAC Group 3 (Legacy K1)

Canada (Alberta)

1989

Canola, Peas, Spring Barley, and Wheat

ethalfluralin, and trifluralin

Inhibition of Microtubule Assembly ( HRAC Group 3 (Legacy K1)

Canada (Manitoba)

1991

Canola, Cropland, Spring Barley, and Wheat

diclofop-methyl, fenoxaprop-ethyl, sethoxydim, and tralkoxydim

Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)

Canada (Saskatchewan)

1991

Canola, Flax, Spring Barley, and Wheat

ethalfluralin, and trifluralin

Inhibition of Microtubule Assembly ( HRAC Group 3 (Legacy K1)

Canada (Manitoba)

1992

Canola, Flax, Spring Barley, and Wheat

diclofop-methyl, ethalfluralin, fenoxaprop-ethyl, sethoxydim, tralkoxydim, and trifluralin

Multiple Resistance: 2 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
Inhibition of Microtubule Assembly ( HRAC Group 3 (Legacy K1)

Canada (Saskatchewan)

1996

Canola, Cropland, Spring Barley, and Wheat

fenoxaprop-ethyl, and sethoxydim

Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)

Canada (Alberta)

1996

Wheat

diclofop-methyl, fenoxaprop-ethyl, and sethoxydim

Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)

Canada (Saskatchewan)

1996

Canola, Peas, Spring Barley, and Wheat

fenoxaprop-ethyl, and trifluralin

Multiple Resistance: 2 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
Inhibition of Microtubule Assembly ( HRAC Group 3 (Legacy K1)

Canada (Ontario)

2001

Corn (maize), and Soybean

flucarbazone-Na, imazethapyr, nicosulfuron, and pyrithiobac-sodium

Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)

Canada (Manitoba)

2002

Wheat

imazethapyr, and sulfosulfuron

Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)

France

1982

Corn (maize)

atrazine

PSII inhibitors - Serine 264 Binders ( HRAC Group 5 (Legacy C1 C2)

France

2011

Corn (maize)

foramsulfuron, and nicosulfuron

Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)

Spain

1987

Corn (maize)

atrazine

PSII inhibitors - Serine 264 Binders ( HRAC Group 5 (Legacy C1 C2)

United States (North Dakota)

1989

Sunflower, and Wheat

trifluralin

Inhibition of Microtubule Assembly ( HRAC Group 3 (Legacy K1)

United States (Wisconsin)

1999

Corn (maize), and Soybean

imazamox

Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)

United States (Montana)

2005

Canola, Peas, Spring Barley, and Wheat

diclofop-methyl, fenoxaprop-ethyl, fluazifop-butyl, pinoxaden, and sethoxydim

Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)

Literature about Similar Cases

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Abit, M. J. M. ; Al-Khatib, K. ; Olson, B. L. ; Stahlman, P. W. ; Geier, P. W. ; Thompson, C. R. ; Currie, R. S. ; Schlegel, A. J. ; Holman, J. D. ; Hudson, K. A. ; Shoup, D. E. ; Moechnig, M. J. ; Grichar, W. J. ; Bean, B. W.. 2011. Efficacy of postemergence herbicides tankmixes in aryloxyphenoxypropionate-resistant grain sorghum. Crop Protection 30 : 1623 - 1628.

The development of aryloxyphenoxypropionate (APP)-resistant grain sorghum could provide additional opportunities for postemergence herbicide grass control in grain sorghum. Field experiments were conducted in Texas (Bushland, and Yoakum), Kansas (Dodge City, Garden City, Hays, Manhattan, Colby, Ottawa, and Tribune), and South Dakota (Highmore) to evaluate the efficacy of quizalofop tank mixes in APP-resistant grain sorghum. Quizalofop was applied alone or in combination with dicamba, 2,4-D, prosulfuron, 2,4-D+metsulfuron methyl, or halosulfuron methyl+dicamba. Herbicides were applied when sorghum was 12-50 cm in height. Overall weed control was greater when quizalofop was applied with other herbicides than when applied alone. At 2 and 4 weeks after treatment (WAT), large crabgrass [Digitaria sanguinalis (L.) Scop.], giant foxtail (Setaria faberi Herrm.), and green foxtail [Setaria viridis (L.) Beauv.] control were greater than 90% when quizalofop was applied alone or in combination with dicamba, halosulfuron methyl+dicamba, or prosulfuron. Palmer amaranth (Amaranthus palmeri S. Wats.), puncturevine (Tribulus terrestris L.), and tumble pigweed (Amaranthus albus L.) control were greater than 90% in all treatments except when quizalofop was applied alone. Herbicide treatments, except those that included 2,4-D, caused slight to no sorghum injury. Grain sorghum yield was greater for all herbicide treatments compared to the weedy check. This research showed that application of quizalofop in combination with broadleaf weed herbicides provided excellent weed control in sorghum..

Darmency, H. ; Picard, J. C. ; Wang, T.. 2011. Fitness costs linked to dinitroaniline resistance mutation in Setaria. Heredity 107 : 80 - 86.

A mutant Thr-239-Ileu at the α2-tubulin gene was found to confer resistance to dinitroanilines, a family of mitosis-disrupting herbicides. However, mutations affecting microtubule polymerization and cell division are expected to impact growth and reproduction, that is, the fitness of a resistant weed or the yield of a tolerant crop, although it has not been demonstrated yet. This study was designed to test this hypothesis for the growth and reproduction of near-isogenic resistant and susceptible materials that were created in F₂ and F₃ generations after a Setaria viridis × S. italica cross. Differential growth was noticeable at the very onset of seedling growth. The homozygous resistant plants, grown both in a greenhouse cabinet and in the field, were smaller and had lower 1000-grain weight and therefore a lower yield. This fitness penalty is certainly due to modified cell division kinetics. Although the presence of the mutant allele accounted for 20% yield losses, there were also measurable benefits of dinitroaniline resistance, and these benefits are discussed..

Bhowmik, P. C.. 2010. Current status of herbicide resistant weeds around the Globe. Journal of Crop and Weed 6 : 33 - 43.

The incidence and wide spread of herbicide resistant weeds is a global problem. Over the past 65 years, repeated use of herbicides has resulted in the evolution of resistant weed species. The first resistant species to triazine was discovered in 1970 in the United States. Since then, a large number of weed species has evolved resistance to several classes of herbicide. Currently, there are 334 resistant biotypes, including 190 weed species (113 dicots and 77 monocots) in over 310, 000 fields around the world Common resistant species are Chenopodium album and Amaranthus retroflexus resistant to triazine, Phalaris minor resistant to isoproturon, P. minor and P. paradoxa resistant to diclofop, Echinochloa colona resistant to propanil, Echinochloa crusgalli resistant to butachlor, Eleusine indica resistant to trifluralin, Lolium rigidum resistant to diclofop, Lactuca serriola resistant to metsuljuron, glyphosate resistance to Eleusine indica, Conyza canadensis, Lolium rigidum, and Lolium multiflorum. Multiple weed resistance to more than one class of herbicides with different modes of action has also been documented with many species. Currently there has been increased herbicide resistance to various weed species around the globe. Most common species are Lolium rigidum, Avena fatua, Amaranthus retroflexus, Chenopodium album, Setaria viridis, Echinochloa crusgalli, Eleusine indica, Kochia scoparia, Conyza canadensis, and Amaranthus hybridus..

Kaundun, S. S.. 2010. An aspartate to glycine change in the carboxyl transferase domain of acetyl CoA carboxylase and non-target-site mechanism(s) confer resistance to ACCase inhibitor herbicides in a Lolium multiflorum population. Pest Management Science 66 : 1249 - 1256.

BACKGROUND: The increasing use of ACCase-inhibiting herbicides has resulted in evolved resistance in key grass weeds infesting cereal cropping systems worldwide. Here, a thorough and systematic approach is proposed to elucidate the basis of resistance to three ACCase herbicides in a Lolium multiflorum Lam. (Italian rye grass) population from the United Kingdom (UK24). RESULTS: Resistance to sethoxydim and pinoxaden was always associated with a dominant D2078G (Alopecurus myosuroides Huds. equivalent) target-site mutation in UK24. Conversely, whole-plant herbicide assays on predetermined ACCase genotypes showed very high levels of resistance to diclofop-methyl for all three wild DD2078 and mutant DG2078 and GG2078 ACCase genotypes from the mixed resistant population UK24. This indicates the presence of other diclofop-methyl-specific resistance mechanism(s) yet to be determined in this population. The D2078G mutation could be detected using an unambiguous DNA-based dCAPS procedure that proved very transferable to A. myosuroides, Avena fatua L., Setaria viridis (L.) Beauv. and Phalaris minor Retz. CONCLUSION: This study provides further understanding of the molecular basis of resistance to ACCase inhibitor herbicides in a Lolium population and a widely applicable PCR-based method for monitoring the D2078G target-site resistance mutation in five major grass weed species..

Wang, T. ; Picard, J. C. ; Tian, X. ; Darmency, H.. 2010. A herbicide-resistant ACCase 1781 Setaria mutant shows higher fitness than wild type. Heredity 105 : 394 - 400.

It is often alleged that mutations conferring herbicide resistance have a negative impact on plant fitness. A mutant ACCase1781 allele endowing resistance to the sethoxydim herbicide was introgressed from a resistant green foxtail (Setaria viridis (L.) Beauv) population into foxtail millet (S. italica (L.) Beauv.). (1) Better and earlier growth of resistant plants was observed in a greenhouse cabinet. (2) Resistant plants of the advanced BC7 backcross generation showed more vigorous juvenile growth in the field, earlier flowering, more tillers and higher numbers of grains than susceptible plants did, especially when both genotypes were grown in mixture, but their seeds were lighter than susceptible seeds. (3) Field populations originating from segregating hybrids had the expected allele frequencies under normal growth conditions, but showed a genotype shift toward an excess of homozygous resistant plants within 3 years in stressful conditions. Lower seed size, lower germination rate and perhaps unexplored differences in seed longevity and predation could explain how the resistant plants have the same field fitness over the whole life cycle as the susceptible ones although they produce more seeds. More rapid growth kinetics probably accounted for higher fitness of the resistant plants in adverse conditions. The likelihood of a linkage with a beneficial gene is discussed versus the hypothesis of a pleiotropic effect of the ACCase resistance allele. It is suggested that autogamous species like Setaria could not develop a resistant population without the help of a linkage with a gene producing a higher fitness..

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