小麦赤霉病及其产生的脱氧雪腐镰刀菌烯醇（DON）毒素严重威胁我国小麦的产量和质量安全。生产中迫切需要既防治赤霉病害又抑制DON毒素的杀菌剂。我们前期研究发现对赤霉病有特效的杀菌剂氰烯菌酯能有效抑制DON毒素形成。研究药剂的作用机制发现，该药剂靶标是病菌肌球蛋白FgMyo1，但其控制毒素形成的机理还不清楚。本项目将重点解析DON毒素合成场所“DON毒素合成小体”的关键组分及其生物学功能，明确氰烯菌酯抑制毒素合成小体形成的机理；阐明氰烯菌酯干扰分子马达FgMyo1复合体，进而阻断DON毒素在细胞内定向转运的分子机制。预期研究结果为后续筛选或研制既防病又抑毒的新型肌球蛋白抑制剂提供科学依据。

Fusarium graminearum, the major causal agent of Fusarium head blight (FHB) disease, results in significant yield loss in infected grains. In addition, it also contaminates the grains with potent mycotoxins such as deoxynivalenol (DON) and its derivatives, harmful to humans, animals. Thus, it is urgent to develop bi-fungicides that could simultaneously suppress FHB disease and reduce DON contamination. Our previous results indicated that phenamacril (JS399-19), a widely used fungicide in China, showed high efficacy against FHB and inhibited DON production. Until now, we have identified that the molecular motor myosin I (FgMyo1) was the drug target of JS399-19. However, the mechanism of DON reduction affected by this fungicide is largely unknown. In this proposal, we will identify components of the DON biosynthesis cellular organelle named "DON-toxisomes", analyze their biological functions, and explore the FgMyo1 mediated-pathway of DON-toxisome traffic in hyphae. Ideally, our prospective results will explain the role of JS399-19 during the toxisomes formation and traffic, and finally determinate the mechanism of JS399-19 in the prevention of DON biosynthesis. The expected accomplishments can provide useful guidance for the development of new fungicides targeting myosin I. It will be benefit for the management of FHB and mycotoxin DON in the future.