组蛋白去乙酰化酶CgHOS2调控胶孢炭疽菌致病力的分子机制研究

由胶孢炭疽菌引起的炭疽病害是造成橡胶树及多种热区作物减产的主要原因之一。组蛋白去乙酰化修饰是一种重要的表观遗传调控方式。目前关于组蛋白去乙酰化酶调控植物病原真菌致病力分子机制的研究还不够深入。申请人前期研究发现，敲除CgHOS2基因对胶孢炭疽菌的生长、产孢没有明显影响；但是敲除突变株对橡胶树叶片的致病力显著下降；进一步分析表明，CgHOS2的缺失会降低病原真菌中黑色素产生，并且影响附着胞的形成。这些结果说明CgHOS2在病原菌对寄主的侵染及寄生过程起着关键作用。本项目将在前期工作基础上，通过转录组及染色质免疫共沉淀-测序手段，预测CgHOS2调控的下游靶标；通过酵母双杂交等方法筛选CgHOS2的互作蛋白；进一步结合遗传学、细胞生物学等方法与技术研究靶标基因的功能。此研究将全面解析CgHOS2调控胶孢炭疽菌致病力的分子机制，为该病原菌的防控提供理论依据。

The anthracnose caused by Colletotrichum gloeosporioides leads to serious economic loss to rubber tree yield and other tropical economic crops. Histone deacetylation is one of the epigenetic regulations. However, the functions and mechanisms of HDAC in regulation of pathogenicity of plant fungal pathogens are still elusive. In the preliminary work, the knock-out mutants of CgHOS2, one of the HDAC coding genes, were generated. Phenotypic analysis showed that although knock-out of CgHOS2 had no obvious influence on vegetative growth and conidiation, the pathogenicity of the mutants were significantly impaired. Further analysis revealed that CgHOS2 is required for melanin biosynthesis and appressorium formation in C. gloeosporioides. These results suggested that CgHOS2 plays important roles in penetration and colonization of C. gloeosporioides to rubber tree leaf. In the following work of the project, we are going to: i) predict the potential targets of CgHOS2 via RNA-seq in combination with ChIP-seq; ii) identify the interacting proteins of CgHOS2 through yeast-two-hybrid; iii) analyze the functions of the predicted targets and interacting proteins. This project will not only figure out the molecular mechanisms of CgHOS2 in regulation pathogenicity, but also provide some clues for developing new control strategy against rubber tree anthracnose.