| 户申奥 1, 2, 薛鑫慧 1, 2, 董佳博 1, 2, 李 赫 3, 贾 硕 3, 马 红 1*, 黄兆峰 2*.内蒙古大豆田反枝苋对乙羧氟草醚的抗性机理及多抗性[J].植物保护,2026,52(4):140-145. |
| 内蒙古大豆田反枝苋对乙羧氟草醚的抗性机理及多抗性 |
| Mechanisms of fluoroglycofen-ethyl resistance and multiple herbicide resistance in Amaranthus retroflexus from soybean fields of Inner Mongolia |
| 投稿时间：2025-08-15 修订日期：2026-01-07 |
| DOI：10.16688/j.zwbh.2025427 |
| 中文关键词: 反枝苋 乙羧氟草醚 抗性机制 靶标位点突变 多抗性 |
| 英文关键词:Amaranthus retroflexus fluoroglycofen-ethyl resistance mechanism target-site mutation multiple resistance |
| 基金项目:生物育种作物病虫草害时空动态与防治策略研究（2024NSZC05）；国家现代农业产业技术体系（CARS-04） |
| 作者 | 单位 | E-mail | | 户申奥 1, 2, 薛鑫慧 1, 2, 董佳博 1, 2, 李 赫 3, 贾 硕 3, 马 红 1*, 黄兆峰 2* | 1. 东北农业大学植物保护学院, 哈尔滨 150030
2. 中国农业科学院植物保护研究所, 北京 100193
3. 内蒙古自治区生物育种技术创新中心, 乌兰浩特 137400 | 马红157492795@qq.com;黄兆峰huangzhaofeng@caas.cn |
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| 中文摘要: |
| 以大豆田中乙羧氟草醚防除失败的反枝苋Amaranthus retroflexus R6346种群为材料, 通过整株生物测定和靶标基因序列扩增等方法, 阐明其对乙羧氟草醚的抗性机制及多抗性特征。结果表明:R6346种群对乙羧氟草醚的抗性指数为15.2;扩增靶标PPX2基因发现第128位氨基酸由Arg突变为Gly。经细胞色素P450抑制剂马拉硫磷预处理后, 该种群的GR_50由56.3 g/hm^2降至43.9 g/hm^2, 抗性水平降低22%。R6346种群对氟磺胺草醚、乳氟禾草灵、噻吩磺隆和灭草松均表现抗性, 但对乙草胺、嗪草酮和异噁草松敏感。本研究表明, R6346种群对乙羧氟草醚的抗性由靶标位点突变(Arg128Gly)和代谢增强共同驱动, 研究结果为科学使用除草剂防控抗性反枝苋提供重要理论依据。 |
| 英文摘要: |
| The R6346 population of Amaranthus retroflexus, collected from soybean fields where fluoroglycofen-ethyl failed to provide effective control, was used as the experimental material. Whole-plant bioassays and target gene sequence amplification were conducted to clarify the resistance mechanism to fluoroglycofen-ethyl and the characteristics of multiple herbicide resistance in this population. The results showed that the resistance index of the R6346 population to fluoroglycofen-ethyl was 15.2. Sequencing of the target gene PPX2 revealed that the amino acid at position 128 was mutated from Arg to Gly. After pretreatment with the cytochrome P450 inhibitor malathion, the GR50 of the R6346 population decreased from 56.3 g/hm 2 to 43.9 g/hm 2, and the resistance level was reduced by 22%. The R6346 population also exhibited resistance to fomesafen, lactofen, thifensulfuron-methyl, and bentazone, but remained susceptible to acetochlor, metribuzin, and clomazone. Our findings indicate that resistance to fluoroglycofen-ethyl in the R6346 population is jointly driven by target-site mutation (Arg128Gly) and enhanced metabolism. These results provide a theoretical basis for the rational use of herbicides to control resistant A.retroflexus populations. |
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