麦角甾醇是真菌细胞膜的重要成分，目前多种杀菌剂（甾醇合成抑制剂，SBIs）靶向于其合成途径的关键酶。甾醇脱甲基抑制剂（DMIs）是SBIs家族最大的一类，作用于甾醇14-α-脱甲基酶，广泛应用于防治真菌病害。SREBP和Upc2是调控甾醇合成及DMIs杀菌剂敏感性的两类主要转录因子，但其同源物在赤霉病菌中均不参与调控甾醇合成及DMIs杀菌剂敏感性。项目前期鉴定出小麦赤霉病菌中一个新的麦角甾醇合成调控的核心转录因子FgSR，其可与蛋白激酶FgSsk2和FgCdc7互作。在此基础上，本项目拟利用蛋白-DNA互作、蛋白-蛋白互作、反向遗传学等手段鉴定赤霉病菌中FgSR的顺式作用元件（SRE）；解析FgSR磷酸化调控麦角甾醇合成及DMIs敏感性机理；鉴定赤霉病菌中麦角甾醇受体，明确其调控麦角甾醇合成的分子机制。预期结果阐述FgSR介导的甾醇合成调控机制，为DMI杀菌剂使用和研发提供科学依据。

Ergosterol is essential fungal membrane lipid components and many kinds of sterol biosynthesis inhibitors (SBIs) target the enzyme of ergosterol biosynthesis pathway. DMIs which inhibit the activity of sterol 14-α-demethylase are the biggest kind of SBIs and were widely used to control both plant and animal fungal disease. In most eukaryotes, sterol biosynthesis is controlled by transcription factor sterol regulatory element binding protein (SREBP) or Upc2. Here, we however found that the SREBP and Upc2 orthologs are not involved in sterol biosynthesis and DMIs sensitivity in Fusarium graminearum. Preliminary results found a transcription factor FgSR (sterol regulator) that may interact with protein kinase FgCdc7 and FgSsk2 to mediate a novel mechanism to regulate ergosterol biosynthesis in Fusarium graminearum. Based on the preliminary results, we will identify the sterol regulatory element (SRE) bond by FgSR, demonstrate the mechanism of phosphorylated FgSR that regulates ergosterol biosynthesis and furthermore identify the receptor of ergosterol in Fuasrium graminerum via reversed genetics, protein-DNA interaction, protein-protein interaction, protein-molecule interaction and other methods. Overall, the upcoming results will elucidate mechanism of sterol biosynthesis regulation mediated by FgSR, and provide theoretical foundation to the application DMIs and drugs development against F. graminearum.