| 植物病原真菌对几类重要单位点杀菌剂的抗药性分子机制 |
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| 引用本文： | 詹家绥,吴娥娇,刘西莉,陈凤平.植物病原真菌对几类重要单位点杀菌剂的抗药性分子机制[J].中国农业科学,2014,47(17):3392-3404. |
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| 作者姓名： | 詹家绥 吴娥娇 刘西莉 陈凤平 |
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| 作者单位： | 福建农林大学植物病毒研究所福建省植物病毒学重点实验室;福建农林大学生物农药与化学生物学教育部重点实验室;中国农业大学农学与生物技术学院植物病理系; |
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| 基金项目： | 农业部公益性行业(农业)科研专项(201303023);福建省自然科学基金(2012J0101) |
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| 摘 要： | 单位点杀菌剂是植物病害管理的重要组成部分，随着单位点杀菌剂的大量、广泛使用，抗性问题也随之产生。目前为止，有植物病原菌对各大类单位点杀菌剂均具抗性的报道。本文作者主要阐述了生产中常用的5类单位点杀菌剂，包括苯并咪唑类杀菌剂（MBCs）、二甲酰亚胺类杀菌剂（DCFs）、14α-脱甲基酶抑制剂（DMIs）、QoIs和琥珀酸脱氢酶抑制剂（SDHIs）的作用机理及抗性分子机制的研究进展，并进一步论述了抗药性产生的机理及抗性治理原则。MBCs作用于β-微管蛋白，抗性主要与靶标蛋白基因的点突变有关，突变造成的氨基酸变化多集中于第50、167、198、200和240等5个位置，主要突变位点为第198位，同一菌株通常只发生一个氨基酸变异，不同位点的点突变甚至同一位点的不同氨基酸替代均会引起抗性水平的差异；DCFs的作用靶标尚不清楚，病原真菌对其抗性可能与双元组氨酸激酶OS基因的点突变有关；DMIs通过抑制14α-脱甲基酶最终影响麦角甾醇的合成，抗性主要与Cyp51的点突变或过量表达或运输体的过量表达相关，Cyp51点突变是抗DMI的主要机制，同一突变对不同的三唑类杀菌剂敏感性表现不尽相同，不同位置的点突变在同一病原菌中对不同三唑类杀菌剂的敏感性影响也不同。点突变数量在不同的真菌中表现不同，有单个发生，也有多个同时发生，且对抗药性具有积累效应；QoIs作用于电子传递链的复合物III，抗性主要与Cytb的点突变有关，与抗性相关的点突变主要发生在Cytb的120—155和255—280两个编码区，其中G143A和F129L为最主要的点突变；SDHIs作用于电子传递链的复合物II，抗性主要与SdhB、SdhC或SdhD的点突变有关，大部分病原真菌对SDHIs的抗性与SdhB点突变有关，SdhB点突变发生位置比较单一，在多种病原菌中突变均发生在相同的组氨酸上即H272, 而SdhC和SdhD突变位点比较多。
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| 关 键 词： | 植物病原真菌 单位点杀菌剂 抗药性 分子机制 |
| 收稿时间： | 2014-03-03 |
Molecular Basis of Resistance of Phytopathogenic Fungi to Several Site-Specific Fungicides |
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| ZHAN Jia-sui,WU E-jiao,LIU Xi-li,CHEN Feng-ping.Molecular Basis of Resistance of Phytopathogenic Fungi to Several Site-Specific Fungicides[J].Scientia Agricultura Sinica,2014,47(17):3392-3404. |
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| Authors: | ZHAN Jia-sui WU E-jiao LIU Xi-li CHEN Feng-ping |
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| Affiliation: | 1、Key Laboratory of Plant Virology of Fujian Province, Institute of Plant Virology, Fujian Agriculture and Forestry University, Fuzhou 350002;
2、Key Laboratory of Biopesticide and Chemical Biology, Ministry of Education, Fujian Agriculture and Forestry University, Fuzhou 350002;
3、Department of Plant Pathology, College of Agriculture and Biotechnology, China Agricultural University, Beijing 100193 |
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| Abstract: | Site-specific fungicides play an important role in plant disease management. However, frequent applications of the fungicides over a large geographic scale can induce the emergence of resistant strains in the pathogen population. Resistance to fungicides with various modes of action has been documented in many plant fungal pathogens. This review summaries the current advances in understanding of the modes of action in five major classes of site-specific fungicides including methyl benzimidazole carbamate (MBCs), dicarboximide fungicides (DCFs), 14α-demethylase inhibitors (DMIs), quinone outside inhibitors (QoIs) and succinate dehydrogenase inhibitors (SDHIs) and the molecular mechanisms of resistance. Evolutionary process of fungicide resistance and management programme aiming to mitigate the emergence of resistance are also discussed in the review. The target protein of MBCs is β-tubulin, and the resistance in phytopathogenic fungi is linked to point mutation in the target protein. Amino acid substitutions in target protein occur mainly at the positions 50, 167, 198, 200, and 240, and the most frequent mutation is amino acid 198. In general, only one substitution occurs in each resistant isolate. Resistant level varies among isolates with different substitutions. The target protein of DCFs has been unknown, the resistance may be correlated with point mutation in histidine kindnase (OS-related) genes. DMIs inhibit sterol 14α-demethylation step in biosynthesis of ergosterol and resistant mechanisms usually include point mutation of Cyp51 or over-expressions of Cyp51 and transporter genes. But point mutation in Cyp51 is the major mechanism of DMI resistance. Different site mutations or even same site and same amino acid substitutions could lead to different resistance to triazoles. The number of point mutations in Cyp51 varies among fungi, ranging from one mutation to several mutations and different mutations have an additive effect on DMI-resistance. QoIs affect the electron transportation chain by binding to complex III and resistance in this type of fungicides is usually linked to point mutation in Cytb occurring usually at amino acids positions 120-155 and 255-280. The most frequent point mutations are G143A and F129L in Cytb. SDHIs inhibit complex II in electron transportation chain. Its resistance is generally related to point mutation either in SdhB, SdhC or SdhD, but in the majority of pathogens, resistance to SDHIs is due to point mutation in H272 of SdhB. In the contrast, the sites of point mutations in SdhC or SdhD vary among different pathogens. |
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| Keywords: | phytopathogenic fungi site-specific fungicide fungicide resistance molecular mechanism |
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