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. Copyright © 2011 Society of Chemical Industry