Molecular basis for resistance to ACCase-inhibiting herbicides in Pseudosclerochloa kengiana populations

• Two Pseudosclerochloa kengiana populations conferred high resistance to fenoxaprop-P-ethyl.
• A Trp-1999-Ser mutation was found in ACCase of the two resistant populations.
• Two dCAPS markers were developed to positively determine the wild type Trp and mutant Ser alleles at ACCase position 1999.

Pseudosclerochloa kengiana is a troublesome annual grass weed of wheat fields in the rice–wheat double cropping areas in China. Resistance has evolved in P. kengiana under continuously selective pressure of ACCase-inhibiting herbicides. Whole-plant experiments showed that two suspected resistant populations 12-SD-12 and 12-SD-13 were highly resistant to fenoxaprop-P-ethyl (69.9- and 57.2-fold); moderately resistant to clodinafop-propargyl (5.9- and 4.1-fold) and pinoxaden (4.4- and 3.5-fold); lowly resistant to fluazifop-P-butyl (2.2- and 2.0-fold) and sethoxydim (1.8- and 1.6-fold), but were sensitive to clethodim (1.0- and 0.9-fold) and mesosulfuron-methyl (1.1- and 0.9-fold). Molecular analyses confirmed that a Trp1999 to Ser mutation was present in the resistant populations. Two dCAPS markers were also developed to positively determine the wild type Trp and mutant Ser alleles at ACCase position 1999. All 350 individual plants of 12-SD-12 population analysed were heterozygous mutants. Meanwhile, 318 mutant heterozygotes and 32 wild types were detected from the 12-SD-13 population. In addition, the analysis of plant genotype and phenotype showed that all wild type plants were killed after treatment with any one of the ACCase-inhibiting herbicides used, while individual plants carrying the W1999S mutation survived except when treated with clethodim. To our knowledge, this is the first report of pinoxaden resistance and a Trp-1999-Ser mutation in the plastid ACCase for P. kengiana.

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