Resistance risk asssement and molecular basis of metconazole in Fusarium pseudograminearum

被引：0
作者：
Li, Guixiang [1 ]
Li, Yiwen [1 ]
Zhang, Ling [1 ]
Jiang, Han [1 ]
Yuan, Kang [1 ]
Miao, Jianqiang [1 ]
Liu, Xili [1 ,2 ]
机构：
[1] Northwest A&F Univ, Coll Plant Protect, State Key Lab Crop Stress Resistance & High Effici, 3 Taicheng Rd, Yangling 712100, Shaanxi, Peoples R China
[2] China Agr Univ, Coll Plant Protect, Dept Plant Pathol, 2 Yuanmingyuanxi Rd, Beijing 100193, Peoples R China
来源：
STRESS BIOLOGY | 2025年 / 5卷 / 01期
关键词：
Metconazole; Resistance mechanism; Resistance risk; Fusarium pseudograminearum; Point mutation; CROWN ROT; SENSITIVITY; WHEAT; TEBUCONAZOLE; CULMORUM; HENAN; GENE; DNA;
D O I：
10.1007/s44154-025-00221-0
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The fungicide metconazole, which acts as a sterol 14 alpha-demethylation inhibitor (DMI), can exhibit strong inhibitory effects on Fusarium pseudograminearum. However, the resistance mechanism as well as the risk that F. pseudograminearum develops resistance to metconazole is yet to be fully assessed. In this study, metconazole displayed a mean EC50 value of 0.0559 mu g/mL against 105 F. pseudograminearum isolates. Ten sensitive parental isolates were then subjected to fungicide adaptation to generate resistant mutants, with in vitro experiments subsequently highlighting the inferior fitness of the mutants. In addition, metconazole exhibited positive cross-resistance with both mefentrifluconazole and tebuconazole. Altogether, the results confirmed the low risk that F. pseudograminearum develops resistance to metconazole. Finally, a mutation genotype (M151T) was identified in FpCYP51B, with the mutants also overexpressing the FpCYP51 genes. Subsequent molecular docking and transformation-based experiments indicated that M151T substitution and overexpression in FpCYP51 genes conferred resistance to metconazole in F. pseudograminearum.
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页数：14
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