由稻瘟病菌引起的稻瘟病严重威胁粮食生产安全。分生孢子萌发形成单个附着胞是稻瘟病菌成功侵染的关键步骤之一。申请人前期通过筛选突变体鉴定到一个控制稻瘟病菌附着胞形成的新基因MoRPI2，编码假定蛋白，其敲除突变体的分生孢子萌发后形成多个附着胞但侵染力显著降低，在雷帕霉素（TOR抑制剂）处理后只形成单个附着胞，表明MoRPI2通过TOR信号途径调控附着胞形成，但其具体机制并不清楚。此外，MoRpi2与可能参与TOR信号途径的磷酸酶MoPsr1存在互作，敲除MoPSR1后分生孢子也形成多个附着胞。在此基础上，本项目将通过一系列细胞学观察、磷酸酶活性分析及雷帕霉素处理等实验，解析MoPsr1在致病过程中的作用，分析MoRpi2是否能被MoPsr1去磷酸化，阐明两者如何调控TOR信号途径进而控制附着胞数量和侵染。研究结果将揭示稻瘟病菌附着胞形成的精细调控机理，为挖掘新型杀菌剂靶标提供理论指导。

Rice Blast, caused by Magnaporthe oryzae, seriously threatens the food security. It is one of the key steps for successful infection of M. oryzae that conidium germinates to form an appressorium. In the preliminary study, MoRPI2, which encodes a protein without any known functional domain, was identified to regulate appressorium formation in M. oryzae, by screening of mutants. MoRPI2 encodes a protein without any known functional domain. The conidia of MoRPI2 deletion mutant formed more than one appressorium per conidium with highly reduced penetration. However, it formed single appressorium when treated with rapamycin, an inhibtor of TOR (Target of Rapamycin). These results suggested that MoRpi2 regulates the appressorium formation by TOR signaling pathway, however, the mechanims remain unclear. Furthermore, MoRpi2 could interact with the phosphatase MoPsr1, which may be involved in the TOR signaling pathway. Notably, ΔMopsr1 also formed more than one appressorium per conidium. Based on this results, this proposed project aims to analyze the function of MoPsr1 during appressorium formation and pathogenicity, reveal whether MoRpi2 can be dephosphorylated by MoPsr1, and explore the mechanism by which MoRpi2 and MoPsr1 regulates TOR signaling pathway to control the number of appressoria and pathogenicity through cytological observation, phosphatase activity analysis, rapamycin treatment and other experiments. The outcome of this project is expected to reveal the precise regulatory mechanism of appressorium formation in M. oryzae, and provide potential targets for the development of new fungicide to control rice blast.