病原微生物碳水化合物酶类因酶解作用，常成为寄主的识别靶点而激发免疫反应，限制了病原的侵染。前期研究发现大丽轮枝菌编码24个偶联了纤维素结合域CBM1的碳水化合物酶类，部分可被寄主识别而激发免疫反应，但删除CBM1后激发免疫反应显著增强，暗示碳水化合物酶类可能通过偶联CBM1结构域以抑制其激发的免疫反应，这一机制未见报道。本项目拟通过大丽轮枝菌CBM1家族蛋白中CBM1结构域抑制免疫反应特性鉴定及毒力贡献分析等研究明确碳水化合物酶类通过偶联CBM1以逃逸其激发免疫反应的特性；利用结构域序列改组、功能位点突变等解析CBM1结构域抑制免疫反应的功能特性；开展CBM1结构域与寄主互作蛋白鉴定及其潜在免疫信号通路调控子分析，阐明CBM1结构域操控免疫反应的信号途径。上述研究将阐明大丽轮枝菌碳水化合物酶类通过偶联CBM1以逃逸免疫反应的分子进化机制，也为作物黄萎病为害机理和防控靶点研究提供理论依据。

The carbohydrate active enzymes (CAZymes) secreted by pathogens usually are recognized by the host plant to stimulate immune response. In a previous study, we determined that there were 24 cellulose binding domain proteins (CBM1) that couple with carbohydrate active enzymes. Of these, there we found part of them induced immune responses, and their ability to stimulate this response was enhanced by the deletion of the corresponding CBM1 motifs. This suggested that CAZymes likely inhibit their ability to stimulate immune response by coupling with the CBM1 motif but the precise mechanism of how this occurs has not been determined. In this project, we plan to explore this mechanism and study its contribution to virulence among members of the Verticillium dahliae CBM1 family. We will study the motif sequence reorganization and mutation of functional site(s) to characterize their function. The identification of interaction proteins from the CBM1 motif and the potential regulators within the immune signaling pathway will be analyzed to illuminate the signaling pathway of CBM1 motif manipulating immune response. This research will illustrate the molecular evolutionary mechanisms of Verticillium dahliae CAZymes escaping immune response by coupling with the CBM1 motif and likely provide the theoretical foundations of pathogenicity mechanisms in Verticillium dahliae that may offer novel targets to control Verticillium wilt.