稻瘟病菌中蛋白激酶MoCK2参与附着胞极性生长影响致病性的初步探索

稻瘟病菌附着胞极性再生是侵染栓形成并导致致病性产生的前提，受到sln1-septin-exocyst的调控，并且这些蛋白在附着胞底部可聚集形成环状结构。本课题前期发现蛋白激酶MoCK2在附着胞中也形成CK2-HRS环状结构，而且与septin环状结构近似于垂直，且出现具有时间先后顺序。基于此，本项目试图解析MoCK2参与附着胞的极性再生，调控侵染栓形成，影响病原菌致病性。拟开展下述研究：（1）观测Δsep3和Δexo70突变体中MoCK2的定位变化，解析sln1-septin-exocyst- MoCK2调控途径；（2）通过pull-down，转录组分析和蛋白磷酸化差异分析筛选MoCK2互作蛋白，并通过酵母双杂交和CO-IP的方式验证；（3）解析互作蛋白功能，完善MoCK2调控网络途径。通过本项目研究，初步理解MoCK2在病原菌致病性产生过程中的作用，为深入开展病害防控提供理论指导。

The re-establishment of polarized growth in appressorium is necessary for the penetration peg formation to cause the pathogenicity in rice blast fungus, Magnaporthe oryzae. This re-establishment is regulated by the sln1-septin-exocyst which can assemble at the bottom of appressorium to form the ring structure. Our preamble research found that the protein kinase MoCK2 can also assemble a ring structure, named CK2-HRS, in the appressorium. The CK2-HRS is perpendicular to the septin-ring structure. What’s more, the formation of CK2-HRS is later than the septin-ring structure presence. Based on these phenomena, we want to elucidate the function of MoCK2 in the re-establishment of polarized growth in appressorium, to regulate the penetration peg formation and to affect the pathogenicity of M. oryzae. The following studies are proposed: (1) detecting the localization of MoCK2 in the Δsep3 and Δexo70 deletion mutant to explain the sln1-septin-exocyst- MoCK2 pathway; (2) screening the proteins interacting with MoCK2 through the pull-down, transcriptome analysis and protein phosphorylation, and verification by the yeast-two -hybrid and CO-IP; (3) analyzing the function of MoCK2- interacting proteins to improve the MoCK2 network. The purpose of our research is understanding the role of MoCK2 in the pathogenicity formation so as to give some theoretical guidance for the agricultural disease control.