{"title":"FgMsn2, a zinc finger transcription factor, regulates stress responses, pathogenicity and metabolism in wheat scab fungus Fusarium graminearum.","authors":"Daiyuan Sun, Chengliang Li, Liangyuan Zhao, Jinling Yang, Haijuan Li, Kaili Duan, Chenfang Wang, Guanghui Wang","doi":"10.1007/s44154-025-00249-2","DOIUrl":null,"url":null,"abstract":"<p><p>Environmental stress adaptation is crucial for the survival and pathogenicity of plant fungal pathogens. In this study, we identified a transcription factor FgMsn2 in Fusarium graminearum, an ortholog of Msn2 in budding yeast. Structural analysis showed that the C2H2 zinc-finger domain is highly conserved across fungi, while other regions are less conserved, suggesting that FgMsn2 may have species-specific functions. Subsequently, we revealed that FgMsn2 is critical for vegetative growth, and conidiogenesis. Deletion of FgMSN2 severely reduced the deoxynivalenol (DON) production and pathogenicity, while enhancing tolerance to oxidative, osmotic, cell wall and membrane stresses. Furthermore, our RNA-seq analysis revealed that FgMsn2 regulates genes involved in energy metabolism, lipid metabolism and stress responses, emphasizing its role in maintaining metabolic balance and stress adaptability. Notably, FgMsn2 influences mitochondrial morphology, as the Fgmsn2 mutant exhibited disrupted mitochondrial structures and reduced ATP production. The Fgmsn2 mutant also showed increased lipid droplet accumulation, indicating the FgMsn2's role in lipid metabolism. Taken together, the FgMsn2 serves as a key regulator in fungal development, plant infection, stress responses, and metabolism. Our study provides valuable insights into the molecular mechanisms of fungal stress adaptation and pathogenicity, suggesting a potential target for the development of more effective fungicides and disease management strategies.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"5 1","pages":"54"},"PeriodicalIF":5.8000,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12401790/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Stress biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/s44154-025-00249-2","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
Environmental stress adaptation is crucial for the survival and pathogenicity of plant fungal pathogens. In this study, we identified a transcription factor FgMsn2 in Fusarium graminearum, an ortholog of Msn2 in budding yeast. Structural analysis showed that the C2H2 zinc-finger domain is highly conserved across fungi, while other regions are less conserved, suggesting that FgMsn2 may have species-specific functions. Subsequently, we revealed that FgMsn2 is critical for vegetative growth, and conidiogenesis. Deletion of FgMSN2 severely reduced the deoxynivalenol (DON) production and pathogenicity, while enhancing tolerance to oxidative, osmotic, cell wall and membrane stresses. Furthermore, our RNA-seq analysis revealed that FgMsn2 regulates genes involved in energy metabolism, lipid metabolism and stress responses, emphasizing its role in maintaining metabolic balance and stress adaptability. Notably, FgMsn2 influences mitochondrial morphology, as the Fgmsn2 mutant exhibited disrupted mitochondrial structures and reduced ATP production. The Fgmsn2 mutant also showed increased lipid droplet accumulation, indicating the FgMsn2's role in lipid metabolism. Taken together, the FgMsn2 serves as a key regulator in fungal development, plant infection, stress responses, and metabolism. Our study provides valuable insights into the molecular mechanisms of fungal stress adaptation and pathogenicity, suggesting a potential target for the development of more effective fungicides and disease management strategies.