<b>HRAC Group 2</b> <font size='2'> (Legacy B) </font> resistant Sinapis arvensis from United States, North Dakota

International Survey of Herbicide-Resistant Weeds

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Thursday, October 31, 2024

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

Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B)

United States, North Dakota

INTRODUCTION		WILD MUSTARD
Wild Mustard (Sinapis arvensis) is a dicot weed in the Brassicaceae family. In North Dakota this weed first evolved resistance to Group 2 (Legacy B) herbicides in 1999 and infests Soybean. 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 cloransulam-methyl, imazethapyr, and thifensulfuron-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 Sep 15, 2000 )
Common Name	Wild Mustard
Species	Sinapis arvensis
Group	Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B)
Herbicides	cloransulam-methyl, imazethapyr, and thifensulfuron-methyl
Location	United States, North Dakota
Year	1999
Situation(s)	Soybean
Contributors - (Alphabetically)	Mike Christoffers, Kirk Howatt, and Richard Zollinger
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ACADEMIC ASPECTS

Confirmation Tests

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

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 Mustard from North Dakota please update the database.

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CONTRIBUTING WEED SCIENTISTS

MIKE CHRISTOFFERS

Associate Professor North Dakota State University Plant Sciences Loftsgard Hall 474A Fargo, 58105, North Dakota United States Email Mike Christoffers Web : Web Site Link

KIRK HOWATT

Associate Professor North Dakota State University Department of Plant Sciences Loftsgard Hall 470F Fargo, 58108-6050, North Dakota United States Email Kirk Howatt Web : Web Site Link

RICHARD ZOLLINGER

Professor and Extension Specialist North Dakota State University Plant Sciences Loftsgard Hall 470H Fargo, 58105, North Dakota United States Email Richard Zollinger 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 Mike Christoffers, Kirk Howatt, and Richard Zollinger 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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