甲基化，泛素化和乙酰化等翻译后修饰在生命体中具有十分重要的作用。其中，组蛋白的乙酰化和去乙酰化与转录调节密切相关。由表观遗传介导的寄主对病原菌的抗性是目前国际上植物与病原菌互作研究领域的一个热点、难点问题。本课题组前期研究结果表明，水稻组蛋白去乙酰化酶OsHDT701通过抑制组蛋白乙酰化水平及PTI相关基因的表达，负调控对稻瘟病菌PAMP诱导PTI的抗性。基于此，本项目将采用分子植物病理学、遗传学、生物化学及生物信息学方法，着重研究OsHDT701在参与抗稻瘟病的调控机制。首先，通过酵母双杂交手段鉴定OsHDT701互作水稻蛋白HDIPs；然后，利用全基因组ChIP-seq分析鉴定OsHDT701蛋白结合的基因启动子区DNA位点；再次，使用RNA-seq分析鉴定OsHDT701的调控谱；最后，系统解析OsHDT701调控水稻抗稻瘟病的信号网络。研究结果将为农作物病害防控策略提供新思路。

Post-translational modifications, such as methylation,ubiquitination, and acetylation play an important role for various biological function. The histone acetylation and deacetylation regulate gene transcription. In general, acetylation of histone is associated with transcriptional activation whereas deacetylation of histione is contributed to gene repression. Epigenetic regulations such as histone modifications and chromatin remodeling are critical for host defense against pathogens. Further understanding of the epigenetic mediated plant resistance, signals and networks and identification of the extent and nature of epigenomic changes induced by different pathogens remain to be elucidated. Our preliminary data showed that OsHDT701 negatively regulates rice blast fungus PAMPs triggered innate immunity by modulating the levels of histone H4 acetylation and the expression of pattern recognition receptor (PRR) and defense-related genes in rice. Therefore, the overall aim of this proposal is understanding the molecular mechanism of OsHDT701 regulating innate immunity in rice. To this aim, firstly,we will perform yeast-two-hybrid assay to screen the OsHDT701 interaction protein. Secondly, identify the OsHDT701 binding DNA sites by a whole-genome ChIP-seq assay. Thirdly, to analysis the OsHDT701 modulated transcriptome by RNA-seq approach. Finally, we will comparing the yeast-two-hybrid, ChIP-seq, and RNA-seq data and find out the signals,networks, and defense-related genes regulated by OsHDT701. Understanding the mechanism of plant epigenetic regulating resistance to pathogens will provide a new strategy for crop disease control.