耿氏硬草对乙酰辅酶A羧化酶类除草剂抗性水平及分子机制初探

为明确耿氏硬草Pseudosclerochloa kengiana(Ohwi)Tzvel潜在抗性种群对不同乙酰辅酶A羧化酶(ACCase)类除草剂的抗性水平及其靶标抗性的分子机制,采用剂量-反应曲线法测定了耿氏硬草对精鰁唑禾草灵、炔草酯、烯禾啶、烯草酮和唑啉草酯5种ACCase类除草剂的抗性水平,扩增并比对了耿氏硬草抗性和敏感种群间ACCase基因的差异。结果显示:与敏感种群SD-6相比,耿氏硬草种群SD-32对精鰁唑禾草灵、炔草酯、烯禾啶、烯草酮和唑啉草酯产生了不同水平的抗性,抗性倍数分别为16.5、7.5、15.0、4.4和5.7;SD-32种群ACCase基因CT区域的2078位氨基酸基因由GAT突变为GGT,导致天冬氨酸(Asp)被甘氨酸(Gly)取代。分析表明,ACCase基因2078位氨基酸的突变可能是导致耿氏硬草对ACCase类除草剂产生抗性的重要原因之一。

Resistance to acetyl-CoA carboxylase-inhibiting herbicides in Pseudosclerochloa kengiana and its molecular resistance mechanism

Whole-plant dose-response experiments were conducted to investigate the resistance levels of the putative resistant Pseudosclerochloa kengiana population to acetyl-CoA carboxylase(ACCase)- inhibiting herbicides. And ACCase gene fragments were amplified, sequenced and compared with the susceptible population, so as to identify its molecular resistance mechanism. The results of whole-plant dose-response assays showed that the putative resistant population SD-32 was resistant to fenoxaprop-pethyl (16.5-fold), clodinafop-propargyl (7.5-fold), sethoxydim (15.0-fold), clethodim (4.4-fold), and pinoxaden (5.7-fold) compared to the reference susceptible population SD-6. Partial chloroplastic ACCase sequences revealed that the resistant population SD-32 possessed an Asp-to-Gly substitution at the ACCase codon position 2078, which resulted from a nucleotide change from GAT to GGT. This study concluded that the change from Asp to Gly mutation at the amino acid position 2078 in the plastid ACCase was an important reason for the resistance to ACCase-inhibiting herbicides in P. kengiana.