Multiple resistant Avena sterilis from United Kingdom

International Survey of Herbicide-Resistant Weeds

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Sunday, December 22, 2024

MULTIPLE RESISTANT STERILE OAT
(Avena sterilis)

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 disrupterHRAC Group 0 (Legacy Z)

United Kingdom

INTRODUCTION		STERILE OAT
Sterile Oat (Avena sterilis) is a monocot weed in the Poaceae family. In United Kingdom this weed first evolved multiple resistance (to 3 herbicide sites of action) in 1993 and infests Cereals, and Wheat. Multiple resistance has evolved to herbicides in the Groups 1 (Legacy A), Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B), and Antimicrotubule mitotic disrupter HRAC Group 0 (Legacy Z). These particular biotypes are known to have resistance to fenoxaprop-ethyl, flamprop-methyl, fluazifop-butyl, imazamethabenz-methyl, iodosulfuron-methyl-Na, mesosulfuron-methyl, and tralkoxydim and they may be cross-resistant to other herbicides in the Groups 1 (Legacy A), Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B), and Antimicrotubule mitotic disrupter HRAC Group 0 (Legacy Z). 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 15, 2013 )
Common Name	Sterile Oat
Species	Avena sterilis
Group	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)
Herbicides	fenoxaprop-ethyl, flamprop-methyl, fluazifop-butyl, imazamethabenz-methyl, iodosulfuron-methyl-Na, mesosulfuron-methyl, and tralkoxydim
Location	United Kingdom
Year	1993
Situation(s)	Cereals, and Wheat
Contributors - (Alphabetically)	Stephen Moss
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NOTES ABOUT THIS BIOTYPE

CROSS RESISTANCE

Stephen Moss

Cross-resistance patterns appear complex in some populations. Resistance to 'Fops' seems to be main problem. The extension person is James Clarke, ADAS Boxworth, Cambridge, CB3 8NN

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ACADEMIC ASPECTS

Confirmation Tests

Field, and Greenhouse trials comparing a known susceptible Sterile Oat biotype with this Sterile 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 1, 2, 0 resistant Sterile 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 multiple resistant Sterile Oat from United Kingdom please update the database.

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CONTRIBUTING WEED SCIENTISTS

STEPHEN MOSS

Iacr - Rothamsted 1076 Ag Sci Bldg PO Box 6108 Harpenden, AL5 2JQ, Hertfordshire United Kingdom Email Stephen Moss

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

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Herbicide Resistant Sterile Oat Globally
(Avena sterilis)

Country

FirstYear

Situation

Active Ingredients

Site of Action

Australia (South Australia)

1989

Canola, Chickpea, Clover, Faba beans, Lentils, Lupins, Peas, and Wheat

diclofop-methyl, fluazifop-butyl, and sethoxydim

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

Australia (New South Wales )

1989

Canola, Chickpea, and Wheat

diclofop-methyl, fluazifop-butyl, and sethoxydim

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

Cyprus

2010

Spring Barley

diclofop-methyl

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)

Greece

2009

Wheat

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

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

Iran

2008

Wheat

pinoxaden

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

Iran

2009

Wheat

iodosulfuron-methyl-Na, and mesosulfuron-methyl

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

Israel

2006

Wheat

clodinafop-propargyl, cycloxydim, and fenoxaprop-ethyl

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

Italy

1992

Wheat

clodinafop-propargyl, cycloxydim, diclofop-methyl, pinoxaden, sethoxydim, and tralkoxydim

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

Italy

2004

Durum wheat

clodinafop-propargyl, cycloxydim, iodosulfuron-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)

Italy

2007

Durum wheat

iodosulfuron-methyl-Na, and mesosulfuron-methyl

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

Spain

2023

Wheat

clodinafop-propargyl, and pinoxaden

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

Turkey

1997

Wheat

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

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

Turkey

2008

clodinafop-propargyl, and pyroxsulam

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)

United Kingdom

1993

Cereals, and Wheat

fenoxaprop-ethyl, flamprop-methyl, fluazifop-butyl, imazamethabenz-methyl, iodosulfuron-methyl-Na, mesosulfuron-methyl, and tralkoxydim

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)

Specific Papers about this Case

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Cocker, K. M. ; Coleman, J. O. D. ; Blair, A. M. ; Clarke, J. H. ; Moss, S. R.. 2000. Biochemical mechanisms of cross-resistance to aryloxyphenoxypropionate and cyclohexanedione herbicides in populations of Avena spp. Weed Research (Oxford) 40 : 323 - 334.

The responses of four UK Avena spp. populations were characterized towards the aryloxyphenoxypropionate (APP) herbicides fenoxaprop-P-ethyl [fenoxaprop-P] and fluazifop-P-butyl [fluazifop-P], and towards the cyclohexanedione (CHD) herbicides cycloxydim and tralkoxydim. An A. sterilis subsp. ludoviciana population (T/41) was found to be highly resistant to fenoxaprop-P-ethyl and fluazifop-P-butyl, but did not show cross-resistance to cycloxydim and tralkoxydim. In contrast, one A. sterilis subsp. ludoviciana (T/11) and one A. fatua population (Dorset) showed partial resistance to both APP herbicides and also showed cross-resistance to the CHD herbicide tralkoxydim, but not to cycloxydim. An enhanced rate of metabolism of fenoxaprop-P-ethyl was found to confer resistance in the two partially resistant Avena populations (T/11 and Dorset), and the presence of an insensitive form of the target enzyme, ACCase [acetyl-coenzyme A carboxylase], was responsible for target site resistance to fenoxaprop-P-ethyl and fluazifop-P-butyl in the highly resistant population T/41. Cross-resistance to the CHD herbicide tralkoxydim in the T/11 and Dorset populations was not conferred by insensitive ACCase, and was most probably caused by enhanced metabolism. This is the first report that resistance to fenoxaprop-P-ethyl can be conferred by enhanced metabolism in Avena spp..

Cavan, G. ; Moss, S. R.. 1997. Herbicide resistance and gene flow in black-grass (Alopecurus myosuroides) and wild-oats (Avena spp.). : 305 - 310.

The process of resistance evolution to fenoxaprop-P-ethyl was investigated in the cereal weeds black-grass (Alopecurus myosuroides) and wild-oats (Avena fatua and Avena sterilis subsp. ludoviciana) at a number of locations in the UK where distinct patches of resistance occur within fields. Genetic fingerprints produced using PCR-based [polymerase chain reaction] techniques did not provide evidence that resistance had spread from one patch to the others. Herbicide-resistant Avena patches contained on average less genetic diversity than herbicide-sensitive counterparts, but all A. myosuroides patches contained similar diversity..

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Literature about Similar Cases

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Saeid Hassanpour-bourkheili, Javid Gherekhloo, Behnam Kamkar, S. Sanaz Ramezanpour. 2021. Mechanism and pattern of resistance to some ACCase inhibitors in winter
wild oat (Avena sterilis subsp. ludoviciana (Durieu) Gillet & Magne) biotypes
collected within canola fields. Crop Protection : 105541 - .

Due to the reports regarding unsuccessful control of Avena sterilis subsp. ludoviciana (Durieu) Gillet & Magne byhaloxyfop-R-methyl in canola fields, the following study was conducted to investigate the resistance of this weed to haloxyfop-R-methyl. Five out of 22 accessions were resistant to haloxyfop-R-methyl. These biotypes were then subjected to various rates of clodinafop propargyl, sethoxydim, pinoxaden and mesosulfuron methyl + iodosulfuron-methyl herbicides and their and cross-resistance to clodinafop propargyl and sethoxydim was confirmed. However, no resistance was observed to pinoxaden and mesosulfuron-methyl + iodosulfuron-methyl herbicides. Indirect study of metabolism by P450 using 1- aminobenzotriazole and piperonyl butoxide showed that this enzyme had no contribution to occurrence of resistance in the studied biotypes. Allele-specific PCR results indicated that Ile-2041-Asn mutation is responsible for resistance of A. sterilis subsp. ludoviciana biotypes, which was confirmed by sequencing of the samples. Since pinoxaden negatively affects canola, the growers face a serious limitation in their choice for chemical management and thus, implementation of integrated weed management such as introduction of row crops such as faba bean in crop rotation and increasing the diversity of herbicide mode of action by cultivation of crops such as sugar beet in crop rotation may prove helpful. In fields under canola-wheat rotation, it is also possible to use pinoxaden in wheat. Also, trifluralin, cycloxydim and clethodim herbicides may be tested on A. sterilis subsp. ludoviciana. This was the first case of A. sterilis subsp. ludoviciana resistance to ACCase inhibitors in canola fields..

Travlos, I. S.. 2013. Competition between accase-inhibitor resistant and susceptible sterile wild oat (Avena sterilis) biotypes. Weed Science 61 : 26 - 31.

Studies were conducted to determine the growth, fecundity, and competitive ability of an acetyl-CoA carboxylase (ACCase)-inhibitor resistant (R) sterile wild oat biotype compared with a susceptible (S) biotype. Seed germination studies indicated that there were no differences in seed germination and seedling vigor between R and S biotypes at any temperature regime. R and S biotypes were grown under noncompetitive and competitive arrangement in the greenhouse. Under noncompetitive greenhouse conditions, growth of the R biotype was similar to that of the S biotype on the basis of plant height, canopy area, and plant biomass. Seed production and weight of R and S plants were also at the same levels. Furthermore, relative competitiveness among the R and S sterile wild oat biotypes was investigated by means of replacement series experiments. The R and S biotypes were compared under seven mixture proportions (6:0,5:1,4:2,3:3,2:4,1:5, and 0:6). No significant differences in competitive ability were observed between R and S biotypes on the basis of plant height, canopy area, or plant biomass. In most cases, relative crowding coefficient (RCC) values at 20, 60, and 100 d after transplanting (DAT) were close to one, indicating equal competitiveness between the R and S biotypes of wild oat used in this competitive study. However, in some cases, the RCC value was 1.31 for plant height, evident of a slight competitive advantage for the R biotype at 100 DAT. In general, ACCase-inhibitor R and S sterile wild oat biotypes were equally competitive, clearly without any growth penalty for R plants in either noncompetitive or competitive conditions..

Papapanagiotou, A. P. ; Kaloumenos, N. S. ; Eleftherohorinos, I. G.. 2012. Sterile oat (Avena sterilis L.) cross-resistance profile to ACCase-inhibiting herbicides in Greece. Crop Protection 35 : 118 - 126.

Sterile oat (Avena sterilis) is the most widely distributed, abundant and harmful weed in the winter cereals grown in Greece. Its effective control has relied for the past three decades upon the ACCase-inhibiting herbicides. However, recently many growers in northern and central Greece have experienced reduced sterile oat control after the application of fenoxaprop-p-ethyl or clodinafop-propargyl. Preliminary screening indicated that less than 80% of the treated plants in 36 and 43 out of 125 sterile oat accessions were killed (R, resistant) by the application of the four times the recommended dose of fenoxaprop-p-ethyl (R-Fx) or clodinafop-propargyl (R-Cd), whereas less than 80% of the treated plants in 29 of them were killed by both herbicides applied at four times the recommended dose. Also, more than 80% of the treated plants in 42 and 35 accessions were killed by the four times the recommended dose (r, partially resistant) of fenoxaprop-p-ethyl (r-Fx) or clodinafop-propargyl (r-Cd), respectively. Finally, more than 80% of the treated plants in 47 and 47 accessions were killed (S, susceptible) by the recommended dose of fenoxaprop-p-ethyl (S-Fx) or clodinafop-propargyl (S-Cd), respectively, whereas more than 80% of the treated plants in 36 of these accessions were killed by the recommended dose of both herbicides. The whole-plant dose-response method used to evaluate 17 R-Fx and five S-Fx accessions showed that 16, 17, 11, and two R-Fx accessions were cross-resistant to clodinafop-propargyl, diclofop-methyl, tralkoxydim, and pinoxaden, respectively. In particular, more than 50% of the treated plants in 12, 12, 17, and three accessions survived the respective application of the four times the recommended dose of fenoxaprop-p-ethyl, clodinafop-propargyl, diclofop-methyl, and tralkoxydim. Regarding pinoxaden, 3, 17 and 20% of the treated plants in three accessions survived its application at four times the recommended dose. All R and the S accessions were effectively controlled by the recommended dose of imazamox and mesosulfuron-methyl+iodosulfuron methyl-sodium. These results strongly suggest that cross-resistance to ACCase-inhibiting herbicides has been developed for sterile oat. Therefore, measures should be taken for crop rotation when possible or rotational use of the available ALS- and ACCase-inhibiting herbicides in order to reduce the potential for development of sterile oat multiple resistance. Regarding the accessions with cross-resistance to APP, CHD and PPZ, these could be effectively controlled by the application of mesosulfuron-methyl+iodosulfuron methyl-sodium..

Kotoula-Syka, E. ; Afentouli, C. ; Georgoulas, I.. 2012. Herbicide-resistant weeds in cereal crops in Greece. : 157 - 161.

In Greece, diclofop-methyl was heavily used for grass weed control whereas chlorsulfuron was used for many years to control broad-leaf weeds in winter cereals. Recently, failures in control of several populations of major weeds were reported in Greece. The objectives of this research were to investigate the possibility of resistance evolution in various populations of Lolium rigidum, Phalaris brachistachys and Avena sterilis to grass herbicides and Papaver rhoeas to chlorsulfuron, and to elucidate the mechanisms of resistance. Plant response to these herbicides was evaluated in pot experiments and laboratory studies. We found that L. rigidum is multiple-resistant to ACCase inhibitors due to an altered target site, and to chlorsulfuron due to enhanced detoxification. Eight biotypes of P. brachystachys, were examined for resistance to ACCase inhibitors and seven of them indicated resistance to fenoxaprop-ethyl. In contrast all eight biotypes were susceptible to tralkoxydim and clodinafop-propargyl. Continuous use of isoproturon resulted in heavy infestation with A. sterilis that tolerates high rates of isoproturon while being susceptible to ACCase inhibitors used. A population of P. rhoeas was found to be resistant to chlosulfuron (altered target site), whereas all P. rhoeas populations were susceptible to imazamox and tolerant to imazapic but resistant plants were cross-resistant to imazethapyr..

Tursun, N.. 2012. Determination on a quick test of herbicide resistance to fenoxaprop-p-ethyl in sterile oat (Avena sterilis L.) in cereal crops. TABAD, Tarım Bilimleri Araştırma Dergisi 5 : 161 - 166.

Sterile oat (Avena sterilis L.) is a major grass weed in cereals in Turkey. Study was determined for quick-test of herbicide resistance to fenoxaprop-p-ethyl in sterile oat (Avena sterilis L.) in a laboratory setting. The experimental design was a randomized plot design with five replications in Petri dishes. Seeds were germinated on 1.3% agar medium whit different proportions hormone (GA3). Then, fenoxaprop-p-ethyle nuron-methyl was added 0 (control), 7.68, 15.36, 30.72, 61.44, 122.88 and 243.76 µM to this solution with. Twenty milliliters of this medium were poured into each Petri dish. Ten seeds were placed into each Petri dish. At the end of study, root and shoot were measured sterile oat seed which germinated and dose-response curves were determined. As a result, it was determined point in time whether herbicides resistance against weeds in a field..

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