Guixiang Li, Yiwen Li, Ling Zhang, Han Jiang, Kang Yuan, Jianqiang Miao, Xili Liu
{"title":"伪谷草镰刀菌对甲康唑的抗性风险评价及分子基础。","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":"{\"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}","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}
Resistance risk asssement and molecular basis of metconazole in Fusarium pseudograminearum.
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.
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