<b>HRAC Group 2</b> <font size='2'> (Legacy B) </font> resistant Sinapis arvensis from Canada, Manitoba

International Survey of Herbicide-Resistant Weeds

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Saturday, December 21, 2024

HRAC GROUP 2 (LEGACY B) RESISTANT WILD MUSTARD
(Sinapis arvensis)

Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B)

Canada, Manitoba

INTRODUCTION		WILD MUSTARD
Wild Mustard (Sinapis arvensis) is a dicot weed in the Brassicaceae family. In Manitoba this weed first evolved resistance to Group 2 (Legacy B) herbicides in 1992 and infests Canola, Cropland, Spring Barley, and Wheat. 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 ethametsulfuron-methyl, and metsulfuron-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 Nov 20, 2000 )
Common Name	Wild Mustard
Species	Sinapis arvensis
Group	Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B)
Herbicides	ethametsulfuron-methyl, and metsulfuron-methyl
Location	Canada, Manitoba
Year	1992
Situation(s)	Canola, Cropland, Spring Barley, and Wheat
Contributors - (Alphabetically)	Lyle Friesen, John O'Donovan, and Rene Van Acker
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NOTES ABOUT THIS BIOTYPE

AREAS FOUND

Lyle Friesen

N.W. Manitoba.

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CONTROL STRATEGIES

Lyle Friesen

There have been 4 or 5 additional ALS inhibitor resistant wild mustard populations identified in southern Manitoba in 2000. Most of these populations are resistant only to ethametsulfuron (Muster) and not to thifensulfuron. Further work to characterize resistance levels and patterns of cross-resistance in these wild mustard populations remains to be done. The importance of ethametsulfuron resistant wild mustard is that these growers can no longer grow conventional canola (in certain fields the wild mustard infestation was very dense), but can only grow genetically engineered herbicide resistant canola.

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GENERAL

Lyle Friesen

Originally selected with chlorsulfuron, thifensulfuron and ethametsulfuron. The wild mustard population is highly resistant to ethametsulfuron methyl, with very slight resistance to metsulfuron methyl, but no resistance to chlorsulfuron, thifensulfuron, imazamethabenz or imazethapyr. The resistance is metabolism-based and is not due to an altered ALS. Resistance became evident after only two applications of ethametsulfuron methyl.

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ACADEMIC ASPECTS

Confirmation Tests

Field, Greenhouse, and Laboratory trials comparing a known susceptible Wild Mustard biotype with this Wild Mustard 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 Mustard 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

Studies on the mechanism of resistance of Group 2 (Legacy B) resistant Wild Mustard from Manitoba indicate that resistance is due to enhanced metabolism. There may be a note below or an article discussing the mechanism of resistance in the Fact Sheets and Other Literature

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 Mustard from Manitoba please update the database.

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CONTRIBUTING WEED SCIENTISTS

LYLE FRIESEN

University Of Manitoba Agriculture Bldg Rua Hugo Cabral 1065 Apto 301 Winnipeg, R3T 2N2, Manitoba Canada Email Lyle Friesen

JOHN O'DONOVAN

Agriculture And Agri-Food Canada Agriculture Bldg Universidad Nacional De Mar Del Plata Ruta Nacional 226, Km 73.5, Beaverlodge, T0H 0C0, Alberta Canada Email John O'Donovan

RENE VAN ACKER

University Of Manitoba Agriculture Bldg 1608 McClaren Dr. Winnipeg, R3T 2N2, Manitoba Canada Email Rene Van Acker

ACKNOWLEDGEMENTS
The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in Manitoba have been instrumental in providing you this information. Particular thanks is given to Lyle Friesen, John O'Donovan, and Rene Van Acker for providing detailed information.

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Herbicide Resistant Wild Mustard Globally
(Sinapis arvensis)

Country

FirstYear

Situation

Active Ingredients

Site of Action

Australia (New South Wales )

1996

Wheat

chlorsulfuron

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

Canada (Ontario)

1983

Corn (maize)

atrazine

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

Canada (Manitoba)

1990

Cropland, Spring Barley, and Wheat

2,4-D, dicamba, dichlorprop, MCPA, mecoprop, and picloram

Auxin Mimics ( HRAC Group 4 (Legacy O)

Canada (Manitoba)

1992

Canola, Cropland, Spring Barley, and Wheat

ethametsulfuron-methyl, and metsulfuron-methyl

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

Canada (Alberta)

1993

Canola, and Spring Barley

ethametsulfuron-methyl, and metsulfuron-methyl

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

Canada (Manitoba)

1994

Cropland, Lentils, and Wheat

metribuzin

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

Canada (Saskatchewan)

2002

Canola, and Cereals

ethametsulfuron-methyl, imazethapyr, thifensulfuron-methyl, and tribenuron-methyl

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

Iran

2009

Winter wheat

iodosulfuron-methyl-Na, metsulfuron-methyl, sulfosulfuron, and tribenuron-methyl

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

Italy

2006

Durum wheat

florasulam, iodosulfuron-methyl-Na, and tribenuron-methyl

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

Spain

2011

Cereals

iodosulfuron-methyl-Na, and tribenuron-methyl

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

Turkey

2001

Wheat

chlorsulfuron

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

Turkey

2008

Wheat

dicamba, propoxycarbazone-Na, thifensulfuron-methyl, triasulfuron, and tribenuron-methyl

Multiple Resistance: 2 Sites of Action
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)
Auxin Mimics ( HRAC Group 4 (Legacy O)

United States (North Dakota)

1999

Soybean

cloransulam-methyl, imazethapyr, and thifensulfuron-methyl

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

Literature about Similar Cases

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Bahmani, A., A. Naderi, E. Zand, M. Masumi, and S. Lack. 2015. Evaluation of selection intensity of acetolactate synthase-inhibitor herbicide resistance endowing Asp-376-Glu mutation in Sinapis arvensis biotype.. Biological Forum 7 : 901 - 905.

In current study we estimated ecological measures of Acetolactate synthase herbicide resistance evolution at lower than recommended dose in Sinapis arvensis herbicide resistance (HR) homozygous for Asp- 376-Glu mutation and herbicide susceptible (HS) biotypes collected from wheat fields in Fars Province, Iran. At low herbicide doses of mesosulfuron + iodosulfuron plants can survive and display quantitative variation in dose-responses. LD50 and GR50 values represented 5.4 and 3-fold ALS resistant than susceptible biotypes. Seed number production per plant showed 3- fold resistance. Linear combination of survival and fecundity values, showed 1 and 0.74 fitness values for (HR) and (HS) biotypes respectively when exposed to the lowdose of 187 g ha-1. With double increasing from 187 to 375 g ha-1 herbicides, fitness decreased by 8-fold in (HS) biotype but reduced slightly by 20% in (HR) biotype. The selection intensity of (HR) at 375 and 187 g ha-1 were 9 and 1.4 respectively. Overall, it is highlighted that evaluation of plant survival and fecundity in assessing mesosulfuron + iodosulfuron selection intensity in the (HR) and (HS) Sinapis arvensis biotypes is a key factor for measuring herbicide resistance evolution..

Warwick, S. I. ; Martin, S. L.. 2013. Gene flow from transgenic oilseed Brassica juncea (L.) Czern. into weedy Sinapis arvensis L. (wild mustard). Plant Breeding 132 : 688 - 693.

Gene flow from acetolactate synthase-resistant (HR) Brassica juncea oilseed canola to related weed, Sinapis arvensis (density 1 plant/m²) was assessed in a 100 m² field plot of HR B. juncea. Two HR F₁ hybrids (H1 and H2) were detected among 109 951 seedlings screened with imazethapyr (hybridization frequency - 1.8×10^-5). Hybridity was confirmed using flow cytometry, B. juncea-specific amplified fragment length polymorphisms (AFLPs) markers, genomic in situ hybridization (GISH) and PCR-based detection of B. juncea's HR gene. H1 and H2 had 2n=27 and 2n=45 chromosomes, corresponding 3x (SrAB) and 5x (SrAABB) genomic structures and reduced male fertility, 3.2 and 16.6% pollen viability, respectively. H1 was self-incompatible, whereas H2 set seed when selfed (B. juncea trait). Selfed F₂, F₃ and F₄ plants showed HR trait persistence and vigorous growth and high (80-100%) pollen fertility in 22% and 39% of the F₂ and F₃ plants, respectively. No progeny were obtained from F₁, F₂ or F₃ hybrids × S. arvensis backcrosses, suggesting the likelihood of introgression of traits is low to negligible..

Mithila, J. ; Hall, J. C.. 2012. Transfer of auxinic herbicide resistance from wild mustard (Sinapis arvensis) into radish (Raphanus sativus) through embryo rescue. Journal of Horticultural Sciences 7 : 29 - 33.

The discovery of auxinic herbicides (e.g., 2,4-D, Dicamba, Picloram) for selective control of broad-leaf weeds in cereal crops revolutionized modern agriculture. These herbicides are inexpensive and do not generally have prolonged residual activity in soil. Although cultivated species of Brassicaceae (e.g., radish and other vegetables) are susceptible to auxinic herbicides, some biotypes of wild mustard (Sinapis arvensis, 2n=18) were found to be highly resistant to Picloram and Dicamba. Inter-generic hybrids between wild mustard and radish (Raphanus sativus, 2n=18) were produced by traditional breeding coupled with in vitro embryo rescue/ovule culture. To increase frequency of embryo regeneration and hybrid plant production, several hundred reciprocal crosses were performed between these species. Upon altering cultural conditions and media composition, a high frequency of embryo regeneration and hybrid plant establishment was achieved. A protocol was also optimized for in vitro clonal multiplication of inter-generic hybrids produced by embryo rescue. To evaluate transfer of auxinic herbicide resistance from wild mustard into hybrid plants, several screening tests (involving in vitro, molecular-based as well as whole plant-based tests) were performed. Results indicated that hybrids of R. sativus × S. arevensis were resistant to auxinic herbicides suggesting, that, the resistance trait was transferred to these hybrids from the wild mustard. This research for the first time demonstrates the possibility of transfer of auxinic herbicide resistance from wild mustard to radish..

Mithila, J. ; McLean, M. D. ; Chen Shu ; Hall, J. C.. 2012. Development of near-isogenic lines and identification of markers linked to auxinic herbicide resistance in wild mustard (Sinapis arvensis L.). Pest Management Science 68 : 548 - 556.

BACKGROUND: Auxinic herbicides are widely used for selective control of many broadleaf weeds, e.g. wild mustard. An auxinic-herbicide-resistant wild mustard biotype may offer an excellent model system to elucidate the mechanism of action of these herbicides. Classical genetic analyses demonstrate that the wild mustard auxinic herbicide resistance is determined by a single dominant gene. Availability of near-isogenic lines (NILs) of wild mustard with auxinic herbicide resistance (R) and herbicide susceptibility (S) will help to study the fitness penalty as well as the precise characterization of this gene. RESULTS: Eight generations of backcrosses were performed, and homozygous auxinic-herbicide-resistant and auxinic-herbicide-susceptible NILs were identified from BC₈F₃ families. S plants produced significantly more biomass and seed compared with R plants, suggesting that wild mustard auxinic herbicide resistance may result in fitness reduction. It was also found that the serrated margin of the first true leaf was closely linked to auxinic herbicide resistance. Using the introgressed progeny, molecular markers linked to auxinic herbicide resistance were identified, and a genetic map was constructed. CONCLUSION: The fitness penalty associated with the auxinic herbicide resistance gene may explain the relatively slow occurrence and spread of auxinic-herbicide-resistant weeds. The detection of the closely linked markers should hasten the identification and characterization of this gene..

Lezáun, J. A. ; Garnica, I. ; Eslava, V.. 2011. Study of a Sinapis arvensis population suspected to be resistant to tribenuron-methyl. : 145 - 148.

A greenhouse trial has been carried out with different herbicides to prove its efficiency on Sinapis arvensis population suspected to be resistant to tribenuron-methyl. The results confirm that this population survives to all rates of tribenuron-methyl treatments tested. However, this population can be controlled with other family of herbicides, such as 2, 4-D 60% and bromoxinil 12%+ioxinil 12%+mcpp-p 36%..

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