Resistance Mechanism to Metsulfuron-Methyl in Polypogon fugax.
Resistance Mechanism to Metsulfuron-Methyl in Polypogon fugax.
复制标题
蓼甲磺隆的抗性机制
DOI：
10.3390/plants10071309
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发表时间：
2021-06-28
期刊：
影响因子：
--
通讯作者：
Lu Y
中科院分区：
文献类型：
--
作者：
Yu X;Wu H;Zhang J;Yang Y;Tang W;Lu Y
短梗水龙骨科是我国及亚洲地区常见的冬季杂草。我们先前已经发现，对乙酰辅酶A羧化酶（ACCase）除草剂具有抗性的白僵菌生物型（R）也不能被一些乙酰乳酸合酶（ALS）除草剂有效地控制。本研究评价了R型油菜对甲磺隆、绿磺隆、单磺隆、吡苯异丙酯4种ALS除草剂的抗性水平及其抗性机制。R型对甲磺隆表现出中等水平的抗性（6.0倍）。ALS基因的序列分析表明，在P. fugax中存在两个ALS基因。然而，在S型和R型之间没有发现与ALS抗性机制相关的ALS基因替换。从R生物型中分离的ALS酶的活性固有地比S生物型更高，并且对甲磺隆的敏感性更低。谷胱甘肽S-转移酶（GST）的活性也不太敏感甲磺隆在R比S生物型。马拉硫磷是一种细胞色素P450（CYP 450）单加氧酶抑制剂，与甲磺隆的协同效应在R植株上比在S植株上大得多，使甲磺隆的ED 50值（抑制50%生长的除草剂剂量）分别降低了23倍和6倍，这表明马拉硫磷介导的代谢增强可能有助于对ALS除草剂的抗性。这些结果表明，甲磺隆抗性的R生物型与上调ALS酶活性和GST和CYP介导的除草剂代谢增强。
Polypogon fugax is a common winter weed in China and other Asia countries. We have previously found a P. fugax biotype (R) resistant to acetyl co-enzyme A carboxylase (ACCase) herbicides also cannot be effectively controlled by some acetolactate synthase (ALS) herbicides. This study evaluated the level of resistance to four ALS herbicides (metsulfuron-methyl, chlorsulfuron, monosulfuron, pyribambenz isopropyl) in the R biotype and the associated resistance mechanism. The R biotype exhibited moderate level of resistance to metsulfuron-methyl (6.0-fold) compared with the sensitive biotype (S). Sequence analysis of ALS gene revealed that two ALS genes existed in P. fugax. However, no substitution associated with ALS resistance mechanism were found in ALS genes between the S and R biotypes. The activity of ALS enzyme isolated from the R biotype was inherently higher and less sensitive to metsulfuron-methyl than the S biotype. Glutathione S-transferases (GST) activity was also less sensitive to metsulfuron-methyl in the R than as the S biotypes. Malathion, a cytochrome P450 (CYP) monooxygenase inhibitor, had much greater synergistic effect with metsulfuron-methyl on the R than as the S plants, reducing the ED50 value (herbicide dose to inhibit growth by 50%) of metsulfuron-methyl by 23- and 6-fold, respectively, suggesting that CYP mediated enhanced metabolism might contribute to the resistance to ALS herbicides. These results suggest that metsulfuron-methyl resistance in the R biotype was associated with the up-regulated ALS enzymatic activity and the GST and CYP-mediated enhanced herbicide metabolism.
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