<b>HRAC Group 2</b> <font size='2'> (Legacy B) </font> resistant Avena fatua from Canada, Saskatchewan

INTERNATIONAL HERBICIDE-RESISTANT WEED DATABASE

HRAC GROUP 2 (LEGACY B) RESISTANT WILD OAT
(Avena fatua)

Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B)

Canada, Saskatchewan

INTRODUCTION		WILD OAT
Wild Oat (Avena fatua) is a monocot weed in the Poaceae family. In Saskatchewan this weed first evolved resistance to Group 2 (Legacy B) herbicides in 1996 and infests Cereals, and Cropland. Group 2 (Legacy B) herbicides are known as Inhibition of Acetolactate Synthase (Inhibition of Acetolactate Synthase ). Research has shown that these particular biotypes are resistant to imazamethabenz-methyl and they may be cross-resistant to other Group 2 (Legacy B) 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 Dec 29, 2000 )
Common Name	Wild Oat
Species	Avena fatua
Group	Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B)
Herbicides	imazamethabenz-methyl
Location	Canada, Saskatchewan
Year	1996
Situation(s)	Cereals, and Cropland
Contributors - (Alphabetically)	Hugh Beckie
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NOTES ABOUT THIS BIOTYPE

GENERAL

Hugh Beckie

Beckie, H. J., A. G. Thomas, A. Légère, D. J. Kelner, R. C. Van Acker, and S. Meers. 1999. Nature, occurrence, and cost of herbicide-resistant wild oat (Avena fatua) in small-grain production areas. Weed Technol. 13:612-625.

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ACADEMIC ASPECTS

Confirmation Tests

Greenhouse trials comparing a known susceptible Wild Oat biotype with this Wild Oat 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 2 resistant Wild Oat 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 2 (Legacy B) resistant Wild Oat from Saskatchewan please update the database.

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CONTRIBUTING WEED SCIENTISTS

HUGH BECKIE

Professor of Crop Weed Science...Canadian Expat University of Western Australia Australian Herbicide Resistance Initiative School of Agriculture and Environment 35 Stirling Highway Crawley, 6009, Western Australia Australia Email Hugh Beckie

ACKNOWLEDGEMENTS
The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in Saskatchewan have been instrumental in providing you this information. Particular thanks is given to Hugh Beckie for providing detailed information.

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Herbicide Resistant Wild Oat Globally
(Avena fatua)

Country

FirstYear

Situation

Active Ingredients

Site of Action

Argentina

2010

Spring Barley, and Wheat

clodinafop-propargyl, diclofop-methyl, and fenoxaprop-ethyl

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

Australia (Western Australia)

1985

Wheat

diclofop-methyl

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

Australia (South Australia)

1988

Canola, Lupins, and Wheat

diclofop-methyl, fluazifop-butyl, haloxyfop-methyl, and tralkoxydim

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

Australia (New South Wales )

1991

Canola, Chickpea, Faba beans, Lentils, Lupins, Spring Barley, and Wheat

clethodim, clodinafop-propargyl, diclofop-methyl, and fenoxaprop-ethyl

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

Australia (New South Wales )

2006

Chickpea, Spring Barley, and Wheat

clodinafop-propargyl, diclofop-methyl, flamprop-methyl, and mesosulfuron-methyl

Multiple Resistance: 3 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)
Antimicrotubule mitotic disrupter ( HRAC Group 0 (Legacy Z)

Australia (Queensland)

2018

Chickpea

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

Belgium

1996

Winter wheat

clodinafop-propargyl, and fenoxaprop-ethyl

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

Brazil

2010

Wheat

clodinafop-propargyl

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

Canada (Alberta)

1989

Cereals, and Spring Barley

difenzoquat, and tri-allate

Multiple Resistance: 2 Sites of Action
Very Long-Chain Fatty Acid Synthesis inhibitors ( HRAC Group 15 (Legacy K3 N)
Cell elongation inhibitors ( HRAC Group 0 (Legacy Z)

Canada (Manitoba)

1990

Canola, Cropland, Spring Barley, and Wheat

clethodim, clodinafop-propargyl, diclofop-methyl, fenoxaprop-ethyl, sethoxydim, and tralkoxydim

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

Canada (Saskatchewan)

1990

Canola, Spring Barley, and Wheat

fenoxaprop-ethyl, and sethoxydim

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

Canada (Alberta)

1991

Canola, and Wheat

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

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

Canada (Manitoba)

1994

Canola, Cropland, Spring Barley, and Wheat

fenoxaprop-ethyl, flamprop-methyl, imazamethabenz-methyl, and rimsulfuron

Canada (Saskatchewan)

1996

Cereals, and Cropland

imazamethabenz-methyl

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

Canada (Saskatchewan)

1996

Wheat

tri-allate

Very Long-Chain Fatty Acid Synthesis inhibitors ( HRAC Group 15 (Legacy K3 N)

Canada (Saskatchewan)

1996

Canola, Lentils, Spring Barley, and Wheat

fenoxaprop-ethyl, imazamethabenz-methyl, and tri-allate

Multiple Resistance: 3 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)
Very Long-Chain Fatty Acid Synthesis inhibitors ( HRAC Group 15 (Legacy K3 N)

Canada (Manitoba)

1997

Wheat

imazamethabenz-methyl

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

Canada (Manitoba)

1997

Wheat

tri-allate

Very Long-Chain Fatty Acid Synthesis inhibitors ( HRAC Group 15 (Legacy K3 N)

Canada (Manitoba)

1997

Wheat

fenoxaprop-ethyl, flamprop-methyl, imazamethabenz-methyl, and tri-allate

Multiple Resistance: 4 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)
Very Long-Chain Fatty Acid Synthesis inhibitors ( HRAC Group 15 (Legacy K3 N)
Antimicrotubule mitotic disrupter ( HRAC Group 0 (Legacy Z)

Canada (Alberta)

1998

Canola, Cereals, and Peas

imazamethabenz-methyl

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

Canada (Alberta)

1998

Canola, Cereals, Peas, and Wheat

fenoxaprop-ethyl, imazamethabenz-methyl, and tri-allate

Canada (Quebec)

2012

Wheat, and Winter barley

fenoxaprop-ethyl, and tralkoxydim

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

Canada (Manitoba)

2015

Spring wheat

fenoxaprop-ethyl, imazamethabenz-methyl, imazapyr, pyroxasulfone, quizalofop-ethyl, sulfentrazone, and tri-allate

Multiple Resistance: 4 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)
Inhibition of Protoporphyrinogen Oxidase ( HRAC Group 14 (Legacy E)
Very Long-Chain Fatty Acid Synthesis inhibitors ( HRAC Group 15 (Legacy K3 N)

Chile

1998

Wheat

clodinafop-propargyl, diclofop-methyl, haloxyfop-methyl, and tralkoxydim

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

France

1996

Wheat

fenoxaprop-ethyl

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

France

2006

Wheat

iodosulfuron-methyl-Na, mesosulfuron-methyl, metsulfuron-methyl, and pyroxsulam

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

Germany

2009

Sugar beets

cycloxydim, fenoxaprop-ethyl, flupyrsulfuron-methyl-Na, mesosulfuron-methyl, and pinoxaden

Multiple Resistance: 2 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)

Germany

2012

Sugar beets

clodinafop-propargyl, fenoxaprop-ethyl, and pinoxaden

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

Iran

2007

Wheat

clodinafop-propargyl, and diclofop-methyl

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

Ireland

2019

Spring Barley, and Winter barley

cycloxydim, pinoxaden, and propaquizafop

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

Mexico

1998

Wheat

clodinafop-propargyl, cycloxydim, diclofop-methyl, fenoxaprop-ethyl, fluazifop-butyl, sethoxydim, and tralkoxydim

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

New Zealand

2014

Clover, and Wheat

fenoxaprop-ethyl, and haloxyfop-methyl

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

Pakistan

2024

Wheat

fenoxaprop-ethyl

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

Poland

2004

Spring Barley, and Spring wheat

diclofop-methyl, fenoxaprop-ethyl, and pinoxaden

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

Poland

2011

Spring Barley, and Spring wheat

iodosulfuron-methyl-Na, mesosulfuron-methyl, propoxycarbazone-Na, and sulfometuron-methyl

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

Poland

2011

Spring Barley, and Spring wheat

fenoxaprop-ethyl, iodosulfuron-methyl-Na, metsulfuron-methyl, pinoxaden, propoxycarbazone-Na, and sulfometuron-methyl

Multiple Resistance: 2 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)

South Africa

1986

Wheat

clodinafop-propargyl, diclofop-methyl, fenoxaprop-ethyl, fluazifop-butyl, imazamox, iodosulfuron-methyl-Na, sethoxydim, sulfosulfuron, and tralkoxydim

Multiple Resistance: 2 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)

Syria

2015

Faba beans, Potatoes, and Wheat

clodinafop-propargyl, and fenoxaprop-ethyl

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

Turkey

2011

Wheat

diclofop-methyl, fenoxaprop-ethyl, and tralkoxydim

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

United Kingdom

1994

Canola, Cereals, and Wheat

fenoxaprop-ethyl, flamprop-m, fluazifop-butyl, imazamethabenz-methyl, mesosulfuron-methyl, pinoxaden, pyroxsulam, and tralkoxydim

United States (Oregon)

1990

Wheat

diclofop-methyl, and fenoxaprop-ethyl

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

United States (Montana)

1990

Spring Barley

difenzoquat, and tri-allate

Multiple Resistance: 2 Sites of Action
Very Long-Chain Fatty Acid Synthesis inhibitors ( HRAC Group 15 (Legacy K3 N)
Cell elongation inhibitors ( HRAC Group 0 (Legacy Z)

United States (Oregon)

1990

Cropland

propyzamide/pronamide

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

United States (Minnesota)

1991

Sugar beets, and Wheat

diclofop-methyl

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

United States (North Dakota)

1991

Cereals, and Wheat

diclofop-methyl, and fenoxaprop-ethyl

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

United States (Washington)

1991

Wheat

diclofop-methyl, fenoxaprop-ethyl, pinoxaden, quizalofop-ethyl, and sethoxydim

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

United States (Idaho)

1992

Cereals, and Wheat

clodinafop-propargyl, diclofop-methyl, and fenoxaprop-ethyl

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

United States (Idaho)

1993

Cereals

difenzoquat, and tri-allate

Multiple Resistance: 2 Sites of Action
Very Long-Chain Fatty Acid Synthesis inhibitors ( HRAC Group 15 (Legacy K3 N)
Cell elongation inhibitors ( HRAC Group 0 (Legacy Z)

United States (Montana)

1996

Cereals

imazamethabenz-methyl

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

United States (North Dakota)

1996

Wheat

imazamethabenz-methyl

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

United States (California)

1996

Spring Barley, and Wheat

difenzoquat

Cell elongation inhibitors ( HRAC Group 0 (Legacy Z)

United States (Colorado)

1997

Spring Barley, and Wheat

diclofop-methyl

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

United States (Montana)

2002

Cropland, Sugar beets, and Wheat

clodinafop-propargyl, diclofop-methyl, fenoxaprop-ethyl, and tralkoxydim

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

United States (South Dakota)

2009

Cereals

fenoxaprop-ethyl

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

United States (South Dakota)

2011

Cereals

mesosulfuron-methyl

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

United States (South Dakota)

2012

Wheat

fenoxaprop-ethyl, and mesosulfuron-methyl

Multiple Resistance: 2 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)

Literature about Similar Cases

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Adamczewski, K. ; Kierzek, R. ; Matysiak, K.. 2013. Wild oat (Avena fatua L.) biotypes resistant to acetolactate synthase and acetyl-CoA carboxylase inhibitors in Poland. Plant, Soil and Environment 59 : 432 - 437.

The aim of the study was to collect seeds of wild oat from the fields where, in spite of the applied herbicides, the weed is very poorly controlled, and to determine under greenhouse conditions if any resistant biotypes are present. In the years 2008-2011, 34 samples of wild oat were collected from fields where the weed was poorly controlled. The biotypes were analyzed in greenhouse experiments to determine if they are resistant to herbicides. Among five resistant biotypes three of them (R3, R4 and R5) were resistant only to iodosulfuron and mesosulfuron, and biotype R2 - only to propoxycarbazone-sodium. Biotype R1 exhibited multiple resistance to iodosulfuron+mesosulfuron and pinoxaden. The use of sulfometuron proves that the mechanism of resistance of two biotypes of wild oat (R1 and R4) to acetolactate synthase inhibitors is associated with target-site mutation. The curve of biotypes R3 and R5 controlled with iodosulfuron+mesosulfuron shows a relatively low resistance index and control of those biotypes with sulfometuron indicates a metabolic resistance..

Augustin, B.. 2013. First report on herbicide resistance of wild oat (Avena fatua L.) in Germany. Journal für Kulturpflanzen 65 : 351 - 354.

Two seed samples of Wild Oat (F1, F2) were collected from sugar beet fields in Rhineland-Palatinate in 2011 showing reduced herbicide performance. A seed treatment with gibberellic acid improved uniform germination of the Wild Oat samples during greenhouse experiments. Herbicide action was tested by means of two successive biotests. ACCase-inhibitors (Fenoxaprop, Pinoxaden, Clodinafop+Pinoxaden, Cycloxidim) and one ALS-inhibitor were treated at 2-3-leafstage of the Wild Oat. The visual rating of herbicide efficiency 3 and 4 weeks after treatment showed a cross resistance among the tested ACCase-inhibitors, except for Cycloxidim for both samples. Seed sample F2 revealed an advanced degree of herbicide resistance, declining from Fenoxaprop to Pinoxaden. Herbicide resistance of sample F1 was restricted to single plants. A subsequent genetic analysis of leaf material revealed a target-site mutation I1781L for both samples of Wild Oat. Further investigations are necessary in order to access reduced performance of Iodosulfuron..

Lehnhoff, E. A. ; Keith, B. K. ; Dyer, W. E. ; Menalled, F. D.. 2013. Impact of biotic and abiotic stresses on the competitive ability of multiple herbicide resistant wild oat (Avena fatua). PLoS ONE 8 : .

Ecological theory predicts that fitness costs of herbicide resistance should lead to the reduced relative abundance of resistant populations upon the cessation of herbicide use. This greenhouse research investigated the potential fitness costs of two multiple herbicide resistant (MHR) wild oat (Avena fatua) populations, an economically important weed that affects cereal and pulse crop production in the Northern Great Plains of North America. We compared the competitive ability of two MHR and two herbicide susceptible (HS) A. fatua populations along a gradient of biotic and abiotic stresses The biotic stress was imposed by three levels of wheat (Triticum aestivum) competition (0, 4, and 8 individuals pot^-1) and an abiotic stress by three nitrogen (N) fertilization rates (0, 50 and 100 kg N ha^-1). Data were analyzed with linear mixed-effects models and results showed that the biomass of all A. fatua populations decreased with increasing T. aestivum competition at all N rates. Similarly, A. fatua relative growth rate (RGR) decreased with increasing T. aestivum competition at the medium and high N rates but there was no response with 0 N. There were no differences between the levels of biomass or RGR of HS and MHR populations in response to T. aestivum competition. Overall, the results indicate that MHR does not confer growth-related fitness costs in these A. fatua populations, and that their relative abundance will not be diminished with respect to HS populations in the absence of herbicide treatment..

Cook, T.. 2013. How widespread is resistance?. Australian Cottongrower 34 : 34, 35 - 39.

This paper presents the results of surveys conducted on the distribution (regardless of herbicide resistance status) in Australia of wild oats [Avena fatua], fleabane [Erigeron], awnless barnyard grass [Echinochloa colona], annual ryegrass [Lolium multiflorum] and windmill grass [Chloris truncata], and their management. The most widespread resistant species are wild oats and fleabane. Awnless barnyard grass and annual rygrass, both resistant to glyphosate, are found mainly in the north and south of the northern cropping region, respectively. The glyphosate-resistant windmill grass is in the infancy of its spread, mainly confined to the central west plains..

Lehnhoff, E. A. ; Keith, B. K. ; Dyer, W. E. ; Peterson, R. K. ; Menalled, F.. 2013. Multiple herbicide resistance in wild oat and impacts on physiology, germinability, and seed production. Agronomy Journal 105 : 854 - 862.

The evolution of weed biotypes resistant to multiple herbicide modes of action, here termed multiple herbicide resistance, is a growing problem around the world. We investigated two multiple herbicide resistant (MHR) wild oat (Avena fatua L.) populations from Montana and hypothesized that they would exhibit fitness costs compared with two herbicide-susceptible (HS) populations. Dose-response tests showed that the MHR populations were resistant to difenzoquat (a membrane disruptor), imazamethabenz (an acetolactate synthase [ALS] inhibitor), flucarbazone (an ALS inhibitor), and tralkoxydim (an acetyl-CoA carboxylase inhibitor). In greenhouse studies, we assessed differences between MHR and HS populations in seed germination, photosynthetic parameters, plant growth, and reproduction. Seeds of one HS population germinated more at cold temperature (4.9°C) and less at high temperature (29.6°C) compared with the other populations. Plants of this HS population also had lower stomatal conductance (23%), intercellular CO₂ concentration (7.5%), and transpiration (15.3%) than the other populations, but there were no differences in photosynthetic rates between any populations. Also, there were no differences in relative growth rate among all HS and MHR populations. The MHR populations initiated seed production several days sooner than the HS populations; however, HS populations produced 67% more tillers, and one HS population ultimately produced 43% more seeds than the MHR populations, indicating a potential fitness cost of resistance. With the exception of seed production differences, our results do not indicate a consistent fitness cost. More research is needed in field settings and with resource competition to further evaluate fitness costs in MHR populations..

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