腐胺促进赤霉病菌DON毒素合成的分子机制

禾谷镰刀菌引起的赤霉病是小麦生产上的毁灭性病害。病菌产生的脱氧雪腐镰刀菌烯醇（DON）不仅严重威胁人畜健康，还帮助病菌在寄主内扩展。病害扩展中DON毒素大量合成，但具体调控机制尚不清楚。项目组前期研究发现病害扩展中寄主产生胁迫应对物质腐胺促进病菌DON合成；腐胺激活次级氮源代谢调控因子FgAreA的转录，使其在DON合成基因（FgTRIs）启动子区富集量增多，增加FgTRIs的表达，进而促进DON合成；组蛋白H2B单泛素化和组蛋白变体H2A.Z的替换参与FgAreA对FgTRIs的转录调控。在此基础上，本项目拟进一步探索腐胺激活转录因子FgAreA的路径，并从表观遗传水平解析FgAreA调控FgTRIs转录的机制，进而设计控毒抑菌的核酸农药。预期结果将丰富禾谷镰刀菌DON毒素合成调控研究，为丝状真菌中表观遗传调控基因转录提供新思路，并为小麦赤霉病防控提供新策略。

Fusarium head blight (FHB) mainly caused by Fusarium graminearum is a devastating disease on wheat. The mycotoxin deoxynivalenol (DON) produced by the pathogen not only threatens food safety, but plays critical roles in disease expansion. After infection, F. graminearum produces substantial DON to help spread within host tissues. But the regulation mechanism of DON biosynthesis during disease expansion is unclear. Our previous study has found that putrescine generated by host promotes DON biosynthesis during disease expansion. Further, we found that putrescine activates the expression of transcription factor FgAreA responsible for secondary nitrogen sources utilization, which increase the enrichment of FgAreA on DON biosynthesis genes (FgTRIs), and then elevates FgTRIs expression resulting in increased DON production. Moreover, we found histone H2B monoubiquitination (H2B ub1) and histone variant H2A.Z substitution are involved in FgAreA-mediated regulation. On the basis, this project aims to explore the function of TOR (Target of rapamycin) pathway in FgAreA activation upon putrescine, elucidate the transcriptional regulation mechanism of FgTRIs regulated by FgAreA via recruiting H2Bub1 and H2A.Z substitution, design nucleic acid fungicides targeting key proteins controlling DON biosynthesis. Results of this study will deepen understanding of DON biosynthesis regulation, provide a novel insight for gene transcription regulated by epigenetics in filamentous fungi, and new strategy for FHB control.