HORSEWEED (Conyza canadensis) with GROUP B/2 resistance: (INHIBITION OF ACETOLACTATE SYNTHASE ) Inhibition of Acetolactate Synthase
MUTATION: ASPARTATE 376 to GLUTAMATE
Horseweed (Conyza canadensis) is a dicot plant in the asteraceae family. A single amino acid substitution from Aspartate 376 to Glutamate has led to resistance to Inhibition of Acetolactate Synthase as indicated in the table below.		Horseweed

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

REFERENCES

Zheng, D. M. ; Kruger, G. R. ; Singh, S. ; Davis, V. M. ; Tranel, P. J. ; Weller, S. C. ; Johnson, W. G.. 2011. Cross-resistance of horseweed (Conyza canadensis) populations with three different ALS mutations. Pest Management Science 67 : 1486 - 1492.

BACKGROUND: Horseweed is a weed commonly found in agronomic crops, waste areas and roadsides. Resistance to ALS-inhibiting herbicides in horseweed was first reported in 1993 in a population from Israel. Resistance to ALS-inhibiting herbicides in horseweed is now widespread, but, as of now, the resistance mechanism has not been reported. RESULTS: Two of three populations evaluated (P116 and P13) were found to be uniform for resistance (>98% of individuals survived 8.8 g AI ha^-1 of cloransulam), whereas a third population, P525, contained about 85% resistant individuals. Cross-resistance to cloransulam, chlorimuron, imazethapyr and bispyribac was observed in the P116 population. P525 and P13 were both sensitive to imazethapyr but resistant to chlorimuron, imazethapyr and bispyribac. Enzyme activity assays indicated that resistance in P13 was due to an altered target site. Southern blot analysis indicated that the ALS target site is encoded by a single copy gene. Overlapping ALS gene regions were amplified and sequenced from each population. Amino acid substitutions of Ser for Pro at position 197 (P197S) was detected from P13, Ala for Pro (P197A) was identified from P525 and substitution of Glu for Asp (D376E) at position 376 was found in P116. Molecular markers were developed to differentiate between wild-type and resistant codons at positions 197 and 376 of horseweed ALS. CONCLUSION: Resistance to ALS-inhibiting herbicides in horseweed is conferred by target-site mutations that have also been identified in other weed species. Identification of the mutations within horseweed ALS gene sequence enables molecular assays for rapid detection and resistance diagnosis..

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

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