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乙酸盐合成酶的3D结构解释了为什么Asp-376-Glu点突变不会给不同的伊米达佐林除草剂带来相同的抵抗水平

Aimone Porri¹, Silvia Panozzo², Mihiret Tekeste Sisay¹

¹BASF SE, Carl-Bosch-Straße 38, 67063 Ludwigshafen am Rhein, Germany.

Pesticide biochemistry and physiology

|September 14, 2024

概括

在杂草中,ALS Asp-376-Glu突变赋予了对imazethapyr的抗性,而不是对imazamox的抗性. 由于特定的分子相互作用,这种差异有助于控制抗除草剂的杂草.

科学领域:

植物科学植物科学
生物化学生物化学
农业科学农业科学

背景情况:

抗除草剂耐药性是一个日益严重的全球问题,由目标部位突变驱动.
抑制乙酸乳酸合成酶 (ALS) 的除草剂被广泛使用,但耐药性正在增加.
艾滋病Asp-376-Glu突变是一种常见的耐药性机制.

研究的目的:

为了评估ALSAsp-376-Glu突变对imazamox和imazethapyr的敏感性差异.
阐明不同除草剂对这种突变的疗效的分子基础.
为抗除草剂作物的杂草管理策略提供信息.

主要方法:

温室剂量反应实验使用阿玛兰 (Amaranthus retroflexus) 和 (Sorghum halepense) 进行.
异质表达突变ALS酶的生物化学抑制和动态表征.
分子对接模拟用于预测除草剂-酶相互作用.

主要成果:

在全植物实验中,Asp-376-Glu突变为imazethapyr提供了高耐药性,但不是imazamox.
生物化学测定证实了ALS突变酶的imazethapyr不敏感性和imazamox敏感性.
对接模拟揭示了ALS活性部位与imazamox的关键基相互作用,与imazethapyr缺席,在ALS活性部位.

结论:

Asp-376-Glu突变对伊米达佐林除草剂的差异性影响是由特定的分子相互作用解释的.
由于独特的结合,伊马扎莫克斯对含有Asp-376-Glu的抗ALS杂草的疗效保持不变.
调查结果为开发有效的杂草耐药性管理和管理指南提供了关键数据.

关键词:

在ALS中,酶的结构与结构是相同的.它们是Asp-376-Glu.抗除草剂耐药性的原因伊米达佐利诺基的存在约翰森格拉斯 (Johnsongrass) 是一个植物.红根猪草是一种红根的猪草.

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