Department of Agricultural and Forest Sciences and Engineering, University of Lleida - Agrotecnio CERCA Center, Lleida, Spain.
Departmento de Agronomia, Universidade Federal de Viçosa, Viçosa, Brazil.
Pest Manag Sci. 2024 Dec;80(12):6041-6052. doi: 10.1002/ps.8373. Epub 2024 Aug 12.
The commercialization of 2,4-D (2,4-dichlorophenoxyacetic acid) latifolicide in 1945 marked the beginning of the selective herbicide market, with this active ingredient playing a pivotal role among commercial herbicides due to the natural tolerance of monocots compared with dicots. Due to its intricate mode of action, involving interactions within endogenous auxin signaling networks, 2,4-D was initially considered a low-risk herbicide to evolve weed resistance. However, the intensification of 2,4-D use has contributed to the emergence of 2,4-D-resistant broadleaf weeds, challenging earlier beliefs. This review explores 2,4-D tolerance in crops and evolved resistance in weeds, emphasizing an in-depth understanding of 2,4-D metabolic detoxification. Nine confirmed 2,4-D-resistant weed species, driven by rapid metabolism, highlight cytochrome P450 monooxygenases in Phase I and glycosyltransferases in Phase II as key enzymes. Resistance to 2,4-D may also involve impaired translocation associated with mutations in auxin/indole-3-acetic acid (Aux/IAA) co-receptor genes. Moreover, temperature variations affect 2,4-D efficacy, with high temperatures increasing herbicide metabolism rates and reducing weed control, while drought stress did not affect 2,4-D efficacy. Research on 2,4-D resistance has primarily focused on non-target-site resistance (NTSR) mechanisms, including 2,4-D metabolic detoxification, with limited exploration of the inheritance and genetic basis underlying these traits. Resistance to 2,4-D in weeds is typically governed by a single gene, either dominant or incompletely dominant, raising questions about gain-of-function or loss-of-function mutations that confer resistance. Future research should unravel the physiological and molecular-genetic basis of 2,4-D NTSR, exploring potential cross-resistance patterns and assessing fitness costs that may affect future evolution of auxin-resistant weeds. © 2024 Society of Chemical Industry.
2,4-D（2,4-二氯苯氧乙酸）拉蒂福利塞在 1945 年的商业化标志着选择性除草剂市场的开始，由于单子叶植物与双子叶植物相比具有天然的耐受性，这种活性成分在商业除草剂中起着关键作用。由于其复杂的作用模式，涉及内源性生长素信号网络的相互作用，2,4-D 最初被认为是一种低风险的除草剂，不会导致杂草产生抗药性。然而，2,4-D 的使用强度增加导致了 2,4-D 抗性阔叶杂草的出现，这挑战了早期的观点。本综述探讨了作物对 2,4-D 的耐受性和杂草进化出的抗药性，强调了对 2,4-D 代谢解毒的深入理解。九种已确认的 2,4-D 抗性杂草物种，由于快速代谢，突显了细胞色素 P450 单加氧酶在 I 相和糖基转移酶在 II 相作为关键酶的作用。对 2,4-D 的抗性也可能涉及与生长素/吲哚-3-乙酸（Aux/IAA）共受体基因突变相关的转运受损。此外，温度变化会影响 2,4-D 的效果，高温会增加除草剂的代谢率并降低杂草的防治效果，而干旱胁迫不会影响 2,4-D 的效果。对 2,4-D 抗性的研究主要集中在非靶标位点抗性（NTSR）机制上，包括 2,4-D 代谢解毒，对这些特性的遗传和遗传基础的研究有限。杂草对 2,4-D 的抗性通常由单个基因控制，要么是显性的，要么是不完全显性的，这引发了关于赋予抗性的功能获得或功能丧失突变的问题。未来的研究应该揭示 2,4-D NTSR 的生理和分子遗传基础，探索潜在的交叉抗性模式，并评估可能影响未来抗生长素杂草进化的适应成本。© 2024 化学工业协会。
