关键词: 植物病原真菌 , 单位点杀菌剂 , 抗药性 , 分子机制

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.

Key words: phytopathogenic fungi , site-specific fungicide , fungicide resistance , molecular mechanism