转录因子FgPacC介导的铁平衡途径调控禾谷镰刀菌致病力的机制研究

禾谷镰刀菌引起的小麦赤霉病及其产生的脱氧雪腐镰刀菌烯醇（DON）毒素严重威胁小麦丰收和农产品质量安全，解析病菌的致病机制对赤霉病的防控具有重要意义。研究发现，禾谷镰刀菌在侵染小麦过程中可感知寄主环境的碱化，调控病菌细胞内铁离子的平衡，进而抵御寄主产生的高铁胁迫，并成功侵染，但目前机制尚不清楚。项目前期研究发现响应pH的转录因子FgPacC负向调控铁吸收基因的表达，进而增强禾谷镰刀菌在碱性条件下对高铁胁迫的耐受力。蛋白激酶FgHal4会对FgPacC磷酸化修饰，影响其功能。这些结果表明FgPacC参与禾谷镰刀菌铁平衡调控过程。项目将进一步解析FgPacC调控铁平衡的分子机制，揭示FgHal4对FgPacC的磷酸化调控机理，阐明FgPacC介导的铁平衡途径在病菌致病过程中的生物学功能。预期结果将为真核生物铁平衡调控的研究提供新视点，为赤霉病的防控提供理论依据。

Fusarium head blight (FHB), predominately caused by Fusarium graminearum, is one of the most devastating diseases of wheat worldwide. Additionally, mycotoxins such as deoxynivalenol (DON) produced by the causal agent poses a serious threat to human health. In the preliminary study, we found that F. graminearum could sense host alkalization to regulate the fungal iron homeostasis, which protects the pathogen from plant-derived high iron levels and thus, increasing fungal infections. However, the underlying regulatory mechanism is largely unknown. In our previous study, we found that FgPacC, the key component of pH signaling pathway, negatively regulate the expression of iron uptake related genes, resulting the increased tolerance to extracellular high iron levels. Further study showed that FgPacC was phosphorylated by kinase FgHal4 in response to high extracellular iron levels. Based on these results, this project aims to uncover the regulatory mechanisms of FgPacC in iron homeostasis of F. graminearum, elucidate the molecular mechanisms of phosphorylation of FgPacC mediated by FgHal4 in responses to ambient pH, and investigate the biological functions of FgPacC-mediated iron homeostasis in fungal development and virulence. Results of this study will provide a novel insight for regulation of iron homeostasis in eukaryote cells and scientific basis for strategy of controlling FHB.