电子传递黄素蛋白ETF调控稻瘟病菌脂肪酸代谢和附着胞功能的机制研究

稻瘟病菌引起的稻瘟病是全球水稻生产的重大病害，对其致病机制的解析一直是植病研究的热点。附着胞是稻瘟病菌的主要侵染机构，而脂肪酸代谢对附着胞形成及致病功能的发挥至关重要。电子传递黄素蛋白ETF及其脱氢酶ETFDH是一类参与线粒体脂肪酸β氧化的电子转运体，前期的研究发现稻瘟病菌ETF及ETFDH突变影响了病菌的生长、产孢及致病性，且突变体不能有效利用外源脂肪酸，然而其具体作用机制尚不清楚。该项目拟从稻瘟病菌ETF和ETFDH突变体脂肪酸代谢水平、附着胞分化及功能、点突变以及蛋白互作等方面展开研究，分析稻瘟病菌电子传递黄素蛋白ETF及其脱氢酶ETFDH介导的脂肪酸代谢及其在病菌生长、产孢、附着胞形成及致病过程中的作用机制。

Rice blast, caused by Magnaporthe oryzae, is the most serious disease of rice production worldwide. Characterizing the mechanism of its pathogenicity has been a hot research topic to date. Appressorium is the major infection structure of M. oryzae, while fatty acid metabolism is crucial to its turgor formation and function. Electron-transferring flavoprotein ETF and its dehydrogenase ETFDH are electron transporters which participate in fatty acid β oxidation. Our previous study demonstrated that mutation of ETF and ETFDH impaired the growth, development and pathogenicity of M. oryzae, and that the mutants could not utilize exogenous fatty acid. However, the function of ETF in regulating regulating fatty acid metabolism and appressorium development remains unknown. The level of fatty acid metabolism and appressorium differentiation in ETF mutant, and function of different FTE protein variants will be investigated here, allowing for the dissection of the ETF mediated fatty acid metabolism and its function in growth, conidiation, appressorium formation and infection process of M. oryzae.