Molecular mechanism of resistance of Fusarium fujikuroi to benzimidazole fungicides
Molecular mechanism of resistance of Fusarium fujikuroi to benzimidazole fungicides
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藤黑镰刀菌抗苯并咪唑类杀菌剂的分子机制
DOI：
10.1111/1574-6968.12504
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发表时间：
2014-08-01
影响因子：
2.1
通讯作者：
Chen, Changjun
中科院分区：
文献类型：
--
作者：
Chen, Zihao;Gao, Tao;Chen, Changjun
虽然多菌肼（MBC）和其他苯并咪唑类杀菌剂过去曾有效防治水稻白僵菌病（由Fusarium fujikuroi、F. proliferatum和F. verticillioides引起），但MBC抗性已成为普遍现象。先前的研究表明，MBC抗性是由F. verticillioides的β(1)-微管蛋白（β (1)tub）基因突变引起的。然而，作为中国的优势种，F. fujikuroi的MBC抗性并非来自β(1)桶的突变。fujikuroi对苯并咪唑类杀菌剂耐药的分子机制尚不清楚。在本研究中，我们确定了尽管富士黑毛菌的β(1)浴盆和β(2)微管蛋白（β(2)浴盆）与verticillioides的β(1)浴盆和β(2)浴盆具有高度同源性，但富士黑毛菌的MBC抗性源于β(2)浴盆[密码子198处GAG(Glu) -> GTG(Val)，密码子200处TTC(Phe) -> TAC (Tyr)，密码子235处GGC(Gly) -> GGT(Gly)]的突变，而不是β(1)浴盆的突变。δ β(2)桶（β(2)桶缺失）突变体对MBC高度敏感，产生的分生孢子较少，毒性低于亲本菌株。将δ β(2)桶型突变体与其亲本菌株的整个β(2)桶型位点的拷贝进行互补，使其对MBC的抗性（或敏感性）恢复到亲本菌株的水平。
Although carbendazim (MBC) and other benzimidazole fungicides have effectively controlled bakanae disease of rice (which is caused by Fusarium fujikuroi, F. proliferatum, and F. verticillioides) in the past, MBC resistance has become common. Previous research has shown that MBC resistance results from a mutation in the beta(1)-tubulin (beta(1)tub) gene in F. verticillioides. However, MBC resistance in F. fujikuroi, a predominant species in China, does not result from a mutation in the beta(1)tub. The molecular mechanism of F. fujikuroi resistance against benzimidazole fungicides is poorly understood. In this study, we determined that although beta(1)tub and beta(2)-tubulin (beta(2)tub) in F. fujikuroi have high homology with beta(1)tub and beta(2)tub in F. verticillioides, MBC resistance in F. fujikuroi results from mutations in beta(2)tub [GAG(Glu) -> GTG(Val) at codon 198, TTC(Phe) -> TAC (Tyr) at codon 200, and GGC(Gly) -> GGT(Gly) at codon 235] but not in beta(1)tub. Delta beta(2)tub (beta(2)tub deletion) mutants were highly sensitive to MBC, produced fewer conidia and were less virulent than parental strains. Complementation of the Delta beta(2)tub mutants with a copy of the whole beta(2)tub locus from their parental strains restored the level of MBC resistance (or sensitivity) to that of the parental strain.