Mechanisms of resistance to fungicides in field strains of Botrytis cinerea
Mechanisms of resistance to fungicides in field strains of Botrytis cinerea
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DOI：
10.1002/ps.566
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发表时间：
2002-09-01
影响因子：
4.1
通讯作者：
Chapeland, F
中科院分区：
文献类型：
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作者：
Leroux, P;Fritz, R;Chapeland, F
灰霉病的病原体灰葡萄孢Pers ex Fr的田间菌株是在1993年至2000年期间从法国葡萄园收集的。根据杀菌剂对芽管伸长和菌丝生长的抑制作用，几种表型已被表征。可检测到两种类型的苯并咪唑耐药菌株（Ben R1和Ben R2）;仅在Ben R1中发现对苯氨基甲酸酯（如乙霉威）的负交叉耐药性。苯并咪唑耐药与β-微管蛋白基因密码子198（Ben R1）或200（Ben R2）的点突变有关。大多数二甲酰亚胺抗性菌株对芳烃类杀菌剂（如敌草胺）也有弱抗性，但对苯基吡咯类杀菌剂（如咯菌腈）仍然敏感。这些抗性田间菌株（Imi R1）在双组分组氨酸激酶基因的第365位含有一个单碱基对突变，可能参与真菌的组氨酸调节。已鉴定出三种苯胺基嘧啶耐药表型。在抗性最强的菌株（Ani R1）中，抗性仅限于苯胺基嘧啶，但在来自Ani R1或野生型菌株的胱硫醚β-裂合酶（这些杀真菌剂的潜在靶位点）的氨基酸序列中没有观察到差异。在其他两种表型（Ani R2和Ani R3）中，抗性扩展到各种其他类别的杀真菌剂，包括二甲酰亚胺，苯基吡咯和甾醇生物合成抑制剂。这种多药耐药可能是由ATP结合盒转运蛋白的过量产生决定的。酰苯胺环酰菌胺是一种新型的杀葡萄孢菌剂，其主要作用位点是参与甾醇C-4去甲基化的3-酮还原酶。除了多重耐药菌株Ani R3外，还发现了其他三种耐环酰菌胺表型。对于其中两个（Hyd R1和Hyd R2），环酰菌胺抗性似乎是由P450介导的解毒作用引起的。靶位点的敏感性降低可能是第三种耐药表型（Hyd R3）中的假定耐药机制。增加的敏感性，甾醇14 α-脱甲基酶抑制剂记录在HydR 1菌株有关的两个氨基酸的变化，在位置15和105的这种酶。(C)2002年，化学工业协会。
Field strains of Botrytis cinerea Pers ex Fr, the causal agent of grey mould diseases, were collected from French vineyards between 1993 and 2000. Several phenotypes have been characterized according to the inhibitory effects of fungicides towards germ-tube elongation and mycelial growth. Two types of benzimidazole-resistant strains (Ben R1 and Ben R2) could be detected; negative cross-resistance to phenylcarbamates (eg diethofencarb) was only found in Ben R1. Benzimidazole resistance was related to point mutations at codon 198 (Ben R1) or 200 (Ben R2) of the beta-tubulin gene. Most dicarboximide-resistant strains were also weakly resistant to aromatic hydrocarbon fungicides (eg dicloran) but remained sensitive to phenylpyrroles (eg fludioxonil). These resistant field strains (Imi R1) contained a single base pair mutation at position 365 in a two-component histidine kinase gene, probably involved in the fungal osmoregulation. Three anilinopyrimidine-resistant phenotypes have been identified. In the most resistant one (Ani R1), resistance was restricted to anilinopyrimidines, but no differences were observed in the amino-acid sequences of cystathionine beta-lyase (the potential target site of these fungicides) from Ani R1 or wild-type strains. In the two other phenotypes (Ani R2 and Ani R3), resistance extended to various other groups of fungicide, including dicarboximides, phenylpyrroles and sterol biosynthesis inhibitors. This multi-drug resistance was probably determined by over-production of ATP-binding cassette transporters. The hydroxyanilide fenhexamid is a novel botryticide whose primary target site is the 3-keto reductase involved in sterol C-4 demethylations. Apart from the multi-drug-resistant strain Ani R3, three other fenhexamid-resistant phenotypes have been recognized. For two of them (Hyd R1 and Hyd R2) fenhexamid-resistance seemed to result from P450-mediated detoxification. Reduced sensitivity of the target site could be the putative resistance mechanism operating in the third resistant phenotype (Hyd R3). Increased sensitivity to inhibitors of sterol 14 alpha-demethylase recorded in Hyd R1 strains was related to two amino-acid changes at positions 15 and 105 of this enzyme. (C) 2002 Society of Chemical Industry.