Target-Site Resistance to Fenoxaprop-P-ethyl in Keng Stiffgrass (Sclerochloa kengiana) from China

Keng stiffgrass is a serious farmland grass weed distributed globally in winter wheat fields and rice–wheat double-cropping areas. The intensive use of acetyl-CoA carboxylase (ACCase)-inhibiting herbicides has led to the evolution of resistance in a growing number of grass weeds. In this study, whole-plant pot bioassay experiments were conducted to establish that a Keng stiffgrass population from eastern China, JYJD-2, has evolved high-level resistance to fenoxaprop- P -ethyl and moderate resistance to quizalofop- P -ethyl and pinoxaden. Using the derived cleaved amplified polymorphic sequence method, a tryptophan-to-cysteine mutation at codon position 1999 (W1999C) was detected in the ACCase gene of the resistant population JYJD-2. Of the 100 JYJD-2 plants tested, we found 47 heterozygous resistant and 53 homozygous sensitive individuals. In vitro ACCase assays revealed that the IC 50 value of the ACCase activity of the resistant population JYJD-2 was 6.48-fold higher than that of the susceptible population JYJD-1. To the best of our knowledge, this is the first report of the occurrence of W1999C mutation in the ACCase gene of fenoxaprop- P -ethyl–resistant Keng stiffgrass. This study confirmed the resistance of Keng stiffgrass to the ACCase inhibitor fenoxaprop- P -ethyl, cross-resistance to other ACCase inhibitors, and the resistance being conferred by specific ACCase point mutations at amino acid position 1999.