WILD MUSTARD (Sinapis arvensis) with GROUP B/2 resistance: (INHIBITION OF ACETOLACTATE SYNTHASE ) Inhibition of Acetolactate Synthase
MUTATION: TRYPTOPHAN 574 to LEUCINE
Wild Mustard (Sinapis arvensis) is a dicot plant in the brassicaceae family. A single amino acid substitution from Tryptophan 574 to Leucine has led to resistance to Inhibition of Acetolactate Synthase as indicated in the table below.		Wild Mustard

Chemical Family	Example Herbicide	Resistance Level
Imidazolinones	Imazethapyr	Resistant > 10 fold
Pyrimidinyl benzoates	Bispyribac-Na	Not Determined
Sulfonylureas	Chlorsulfuron	Resistant > 10 fold
Triazolopyrimidine - Type 1	Chloransulam-methyl	Resistant > 10 fold
Triazolinones	Flucarbazone-Na	Resistant > 10 fold

REFERENCES

Christoffers, M. J. ; Nandula, V. K. ; Howatt, K. A. ; Wehking, T. R.. 2006. Target-site resistance to acetolactate synthase inhibitors in wild mustard (Sinapis arvensis). Weed Science 54 : 191 - 197.

Inhibitors of acetolactate synthase (ALS) are important herbicides for control of wild mustard, a common weed of the north central United States and Canada. Wild mustard that survived treatments with the ALS inhibitors cloransulam, imazethapyr and thifensulfuron was sampled from a North Dakota soyabean field in 1999. The mechanism of resistance and response of this wild mustard biotype to ALS-inhibiting herbicides was investigated. In vitro enzyme-inhibition experiments confirmed a resistance mechanism associated with the ALS enzyme; imazethapyr or imazamox at 1×10^-4 M caused only 10-11% and 12-16% reductions in ALS activity, respectively. ALS from a susceptible wild mustard biotype was inhibited by 50% (I₅₀) with imazethapyr at 8×10^-7 M or imazamox at 1.1×10^-6 M. Whole-plant greenhouse treatments confirmed cross-resistance across ALS-inhibitor classes. Treatment with twice-normal field rates of thifensulfuron, ethametsulfuron, triflusulfuron, imazamox, imazethapyr, flumetsulam, cloransulam, flucarbazone and imazamethabenz reduced biomass of the susceptible biotype by at least 96% at 28 d after treatment. Biomass of the resistant biotype was reduced by 49% with triflusulfuron and 35% with thifensulfuron, but was not reduced with other herbicides. DNA sequence analysis of ALS genes from resistant and susceptible biotypes revealed a point mutation inferring a Trp-to-Leu amino acid substitution in ALS of the resistant biotype. This mutation, corresponding to position 574 of the Arabidopsis ALS amino acid sequence, is known to confer cross-resistance to ALS-inhibiting herbicides and is the probable cause of resistance in the wild mustard biotype. Phylogenetic analysis of wild mustard and rape ALS sequences confirmed that the Trp₅₇₄ mutation arose within wild mustard and was not derived via introgression from imidazolinone-resistant rape. The results of this research indicate a naturally occurring target-site point mutation responsible for conferring cross-resistance to ALS-inhibiting herbicides in this wild mustard biotype..

Warwick, S. I. ; Sauder, C. ; Beckie, H. J.. 2005. Resistance in Canadian biotypes of wild mustard (Sinapis arvensis) to acetolactate synthase inhibiting herbicides. Weed Science 53 : 631 - 639.

Multiple cases of ALS inhibitor-resistant weed biotypes are reported for many species, including wild mustard. The physiological extent and molecular basis of resistance to ALS inhibitors was compared in 4 wild mustard biotypes from western Canada: a sulfonylurea (SU)-resistant (R) biotype from Manitoba detected in 1992; an SU (ethametsulfuron)-R biotype from Alberta detected in 1993 (metabolism-based resistance); an SU-R biotype from Manitoba detected in 2002; and a SU- and imidazolinone (IMI)-R biotype from Saskatchewan detected in 2002. Herbicide dose-response experiments confirmed that the 2 Manitoba biotypes were resistant to the SU herbicides ethametsulfuron and tribenuron:thifensulfuron mixture, whereas the Saskatchewan biotype was resistant to both SU herbicides and to imazethapyr, an IMI herbicide. Sequence analysis of the ALS gene detected target site mutations in 3 of the 4 R biotypes, with amino acid substitutions Pro₁₉₇ to Ser (Domain A of the gene) in the 2 SU-R Manitoba biotypes and Trp₅₇₄ to Leu (Domain B) in the Saskatchewan biotype. The Alberta SU-R biotype had the same ALS nucleotide and amino acid sequence as the susceptible population at these 2 positions. Two heterozygous individuals [Trp₅₇₄ (Tt/gG)] were detected in the Saskatchewan biotype, and genetic segregation for nucleotide bases and resistance phenotype was consistent with single gene control. Nucleotide variation in neutral regions of the ALS gene varied with biotype, with no variation in the 2 Manitoba biotypes, 2 variants in the Saskatchewan biotype and 16 neutral nucleotide polymorphisms (0.9%) in the Alberta biotype. The occurrence of at least 3 different ALS inhibitor-R biotypes in this important weed species is likely to impact negatively on the use of ALS inhibitors, such as the IMIs, and serves as a warning for strict implementation of herbicide rotations to prevent or delay the evolution and spread of such populations..

This case was entered by Patrick Tranel Email: tranel@illinois.edu

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