植物病原真菌对甾醇脱甲基抑制剂类杀菌剂抗性分子机制研究进展

Research progress on molecular resistance mechanism of plant pathogenic fungi to sterol demethylase inhibitors

甾醇脱甲基抑制剂(DMI)可通过抑制病原真菌的14α-去甲基化酶(CYP51)而干扰或阻断细胞膜麦角甾醇的生物合成,造成有毒甾醇积累,从而影响细胞膜的结构及功能,进而发挥抗菌作用。随着DMI类杀菌剂的广泛应用,病原菌对其的抗性问题日益严重。本文从抗药性分子机制出发,总结出病原菌对DMI类杀菌剂产生抗性的主要原因为:CYP51氨基酸突变引起其与杀菌剂间的亲和力下降;启动子区域基因片段的插入引起CYP51基因过表达;转录因子激活突变或启动子区域基因片段插入导致外排蛋白基因过表达。本文基于杀菌剂的作用方式及病原菌抗性机制研究展开综述,可为杀菌化合物的结构修饰与优化、新靶点改进和研发以及病原真菌的抗药性治理提供参考。

Sterol demethylase inhibitors(DMIs)inhibit the activity of C-14αdemethylase,interfere with or block the biosynthesis of ergosterol in cell membrane,cause the accumulation of toxic sterol,affect the structure and function of cell membrane,and thus exert antifungal activities.With the widespread application of DMI fungicides,plant pathogens exhibit arisen resistance to these compounds.Here,we discussed the molecular mechanisms of DMI resistance in agriculture and summarized the main causes of the resistance as follows:Point mutations of CYP51 amino acid residues decrease affinity with fungicides;The insertions of sequence in promoter region lead to overexpression of CYP51 gene;Transcriptional activation or sequence insertion in promoter region promotes the overexpression of efflux pump proteins.This study performed an overview of DMI mode actions and molecular resistance mechanism,which will provide a reference for the structural modification and optimization of antibacterial compounds,and strategies for the discovery of new target proteins,promoting the sustainable fungicide innovation and the breakthrough in the resistance issues.