Abstract

The intensive and global application of ACCase-inhibiting herbicides has resulted in the evolution of resistance in a growing number of grass weeds. Among the mutations implicated in conferring resistance, limited knowledge is available regarding mutations at codon position 1999. In addition, multiple copies of genes encoding plastidic ACCase have been ignored in previous studies of resistance in Alopecurus japonicus. Dose-response tests indicated that the population JLGY-4 had evolved high-level resistance to fenoxaprop-P-ethyl. The carboxyltransferase domain of the ACCase gene in A. japonicus was sequenced and compared. Two loci encoding plastidic ACCase were isolated from both the resistant and sensitive populations. Simultaneously, two resistance-endowing mutations at codon position 1999 of ACCase were determined (W1999C and W1999L). Moreover, a molecular study was conducted to determine the mechanism of resistance to some ACCase-inhibiting herbicides. The W1999C mutation conferred resistance to fenoxaprop and moderate resistance to pinoxaden. The W1999L mutation conferred resistance to fenoxaprop. This study revealed that A. japonicus had multiple copies of genes encoding plastidic ACCase, and each gene was able to carry its own mutation. It also established the clear importance of the W1999C and W1999L mutations in conferring resistance to ACCase-inhibiting herbicides.

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