疫霉菌可以分泌大量效应子到寄主细胞中，通过多种途径来操控植物抗病性进而成功致病。申请人前期研究发现大豆疫霉RxLR效应子PsAvh262能够稳定内质网应激调节因子BiP，并抑制寄主内质网应激诱导的细胞死亡，但其具体作用机制尚不清楚。近期我们发现效应子PsAvh262与内质网分子伴侣BAG7互作，而BAG7能与BiP结合调控内质网应激反应并促进疫霉菌的侵染。本项目拟通过研究PsAvh262与大豆BAG7之间的互作机制，明确BAG7在内质网应激和植物免疫中的功能，探索效应子对BAG7重定位和修饰的影响，阐明效应子PsAvh262与寄主BAG7结合的生化效应与致病机理。本研究的完成将进一步揭示疫霉菌利用效应子挟持寄主内质网应激这一致病机制，有助于认识疫霉菌侵染与寄主内质网应激调控的关系，为合理有效地开发卵菌病害控制技术奠定理论基础。

Phytophthora pathogens secrete an array of specific effector proteins to manipulate host innate immunity in multiple ways to promote pathogen colonization. Our previous study shows that a Phytophthora RxLR effector targets plant BiP, the master regulators of the ER stress, to manipulate the ER stress pathways and suppress ER stress-induced programmed cell death to promote infection. Recently, we found that Phytophthora sojae effector PsAvh262 interacts with BAG7, which the BAG7 binds to BiP for manipulating the ER stress response and promotes Phytophthora infection. Here, the molecular and virulent mechanism of the PsAvh262-BAG7 interaction will be studied, including: the function of BAG7 in regulating host resistance to Phytophtora and ER stress, the impact of PsAvh262 in the translocation and cleavage of BAG7 to illustrate the binding mechanism, the role of BAG7 in the regulating ER stress and host resistance of PsAvh262 and the elucidation of the virulent mechanism of the PsAvh262-BAG7 interaction. This work focuses on how Phtophthora utilizes effector to hijack host ER stress, which will further illuminate this mechanism that effector is able to hijack and overcome host ER stress, understand the relationship between Phytophthora infection and host ER stress, and provide scientific basis for development of novel control strategies against oomycete pathogens.