日本看麦娘对精噁唑禾草灵和甲基二磺隆的抗性机制

为明确抗性日本看麦娘种群对精噁唑禾草灵和甲基二磺隆的抗性机制,研究了乙酰辅酶A羧化酶(acetyl-CoA carboxylase,ACCase)和乙酰乳酸合成酶(acetolactate synthase,ALS)基因在抗性和敏感日本看麦娘种群内的差异,以及谷胱甘肽-S-转移酶(glutathione S-transferases,GSTs)的活性差异,同时测定了抗性种群AFT对不同的ACCase和ALS抑制剂类除草剂的交互抗性。结果显示:与敏感种群AH-7相比,抗性种群AFT的ACCase基因CT区的2027位氨基酸和ALS基因的574位氨基酸发生突变;AFT种群的GSTs活性经过精噁唑禾草灵和甲基二磺隆处理后明显增强,且显著强于敏感种群AH-7;抗性种群AFT对炔草酯、烯草酮、氟唑磺隆的抗性倍数分别为27.90、34.43、10.30,表现出高水平的抗性,对唑啉草酯、甲咪唑烟酸、双草醚的抗性倍数分别为5.49、6.42、5.01,表现出中等水平的抗性。经除草剂诱导后,植株体内基于GSTs代谢酶介导的代谢反应水平升高,加快植株对除草剂的代谢解毒反应;抗性种群AFT的ACCase基因和ALS基因中发生的氨基酸突变和GSTs活性的增强可能是其产生抗药性的重要原因。

Resistance mechanism of Alopecurus japonicus in response to fenoxaprop-P-ethyl and mesosulfuron-methyl

To clarify the resistance mechanism of Alopecurus japonicus to fenoxaprop-P-ethyl and mesosulfuron-methyl, fragments encoding acetyl-CoA carboxylase (ACCase) and acetolactate synthase (ALS) were amplified, cloned and sequenced from resistant (R) and susceptible (S) populations of A. japonicus, respectively. Activity differences of glutathione S-transferases in R and S populations were studied. Dose-response experiments were conducted to evaluate the resistance levels of resistant A. japonicus population to different ACCase-and ALS-inhibiting herbicides. The nucleotide sequence analysis showed that a substitution of tryptophan acid (Trp) 2027 by cysteine acid (Cys) existed in the CT domain of ACCase gene, and a substitution of tryptophan acid (Trp) 574 by arginine acid (Arg) of ALS gene existed in AFT population. The level of metabolic response mediated by GSTs metabolizing enzymes in plants was increased after herbicide treatment, the metabolic detoxification response of plants to herbicides was accelerated, the GSTs activity of R was obviously higher than that of S population. A. japonicus AFT population confered high resistance to clodinafop-propargyl, clethodim, flucarbazone-Na with resistance index of 27.90, 34.43 and 10.30, respectively. Moderate resistance to pinoxaden, imazapic, bispyribac-sodium with resistance index of 5.49, 6.42 and 5.01. This study indicated that the substitutions of tryptophan acid at position 2027 in the ACCase gene, tryptophan acid at position 574 in the ALS gene and the significantly increased of GSTs activity might be linked to resistance to fenoxaprop-P-ethyl and mesosulfuron-methyl in AFT populations.