Metabolism of 2,4-D in plants: comparative analysis of metabolic detoxification pathways in tolerant crops and resistant weeds.
IF 3.8
1区 农林科学
Q1 AGRONOMY
Joel Torra, Ricardo Alcántara-de la Cruz, Marcelo Rodrigues Alves de Figueiredo, Todd A Gaines, Mithila Jugulam, Aldo Merotto, Candelario Palma-Bautista, Antonia M Rojano-Delgado, Dean E Riechers
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Abstract
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 在植物体内的代谢:耐受性作物和抗性杂草代谢解毒途径的比较分析。
1945 年,2,4-D(2,4-二氯苯氧乙酸)利福膦的商业化标志着选择性除草剂市场的开始,由于单子叶植物比双子叶植物具有天然耐受性,这种活性成分在商业除草剂中发挥着举足轻重的作用。由于 2,4-D 的作用模式复杂,涉及内源辅助素信号网络的相互作用,因此最初被认为是一种杂草抗药性演变风险较低的除草剂。然而,随着 2,4-D 使用量的增加,出现了对 2,4-D 产生抗性的阔叶杂草,这对以前的看法提出了挑战。本综述探讨了作物对 2,4-D 的耐受性和杂草的抗性演变,重点是深入了解 2,4-D 的代谢解毒过程。九种经证实的 2,4-D 抗性杂草是由快速新陈代谢驱动的,其中第一阶段的细胞色素 P450 单氧化酶和第二阶段的糖基转移酶是关键酶。对 2,4-D 的抗性还可能与辅助素/吲哚-3-乙酸(Aux/IAA)共受体基因突变导致的转运障碍有关。此外,温度变化也会影响 2,4-D 的药效,高温会提高除草剂的代谢率,降低除草效果,而干旱胁迫则不会影响 2,4-D 的药效。对 2,4-D 抗性的研究主要集中在非靶标抗性(NTSR)机制上,包括 2,4-D 代谢解毒,而对这些性状的遗传和基因基础的探索有限。杂草对 2,4-D 的抗性通常由一个显性或非完全显性的单基因控制,这就引起了有关赋予抗性的功能增益突变或功能缺失突变的问题。未来的研究应揭示 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助剂杂草进化的适应性成本。© 2024 化学工业协会。
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