Resistance risk asssement and molecular basis of metconazole in Fusarium pseudograminearum.

IF 5.8
Guixiang Li, Yiwen Li, Ling Zhang, Han Jiang, Kang Yuan, Jianqiang Miao, Xili Liu
{"title":"Resistance risk asssement and molecular basis of metconazole in Fusarium pseudograminearum.","authors":"Guixiang Li, Yiwen Li, Ling Zhang, Han Jiang, Kang Yuan, Jianqiang Miao, Xili Liu","doi":"10.1007/s44154-025-00221-0","DOIUrl":null,"url":null,"abstract":"<p><p>The fungicide metconazole, which acts as a sterol 14α-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 EC<sub>50</sub> value of 0.0559 μg/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.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"5 1","pages":"30"},"PeriodicalIF":5.8000,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12043553/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Stress biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/s44154-025-00221-0","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

The fungicide metconazole, which acts as a sterol 14α-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 μg/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.

伪谷草镰刀菌对甲康唑的抗性风险评价及分子基础。
杀菌剂metconazole作为一种甾醇14α-去甲基化抑制剂(DMI),对pseudograminearum镰刀菌有较强的抑制作用。然而,对该菌的耐药机制以及对甲康唑产生耐药性的风险尚未得到充分的评估。在本研究中,甲康唑对105株伪谷草镰刀菌的EC50平均值为0.0559 μg/mL。然后对10个敏感亲本分离物进行杀菌剂适应以产生抗性突变体,随后的体外实验突出了突变体的低适应性。此外,甲康唑与甲苯三氟康唑和戊康唑均表现出正交叉抗性。综上所述,结果证实假谷草镰刀菌对甲康唑产生抗性的风险较低。最后,在FpCYP51B中发现了一个突变基因型(M151T),该突变体也过表达FpCYP51基因。随后的分子对接和转化实验表明,FpCYP51基因的M151T替代和过表达使假禾草菌对甲康唑产生抗性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
3.10
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信