草莓果实与灰葡萄孢（Botrytis cinerea）互作下的细胞壁信号模式及诱导抗性响应机制

灰葡萄孢（Botrytis cinerea）引起的灰霉病是引起草莓采后损失的重要因素。研究B. cinerea侵染下草莓果实抗性响应规律，可为寻找外源调控手段提供依据。病原菌果胶酶（PGs）与植物果胶酶抑制蛋白（PGIPs）互作降解植物细胞壁产生的寡聚半乳糖醛酸（OGs）是激发植物系统抗性的重要信号之一，但B. cinerea侵染下草莓果实OGs信号模式及其作用机制尚不明确。本项目拟分析B. cinerea侵染下细胞壁结构特点及OGs组分特征，通过外源OGs处理明晰诱导系统抗性产生的关键OGs信号组分；构建基因敲除突变株BcPG1和FaPGIP-BcPG1瞬时遗传转化果实，比较细胞壁结构特点及OGs组分特征，明确OGs信号产生的调控机制；分析OGs介导下的次生代谢网络，从抗病应答的物质代谢途径解析OGs信号的作用模式。最终明确草莓果实与B. cinerea互作下OGs信号特征及其作用机制。

Gray mold caused by Botrytis cinerea is the important factor causing postharvest strawberry fruit losses. Study on the resistance response of strawberry fruit under B. cinerea infection can provide information for postharvest intervention technologies. Oligogalacturonide (OGs) produced by the interaction of pathogen polygalacturonases (PGs) and plant polygalacturonase inhibitor proteins (PGIPs) to degrade plant cell wall is one of the important signals to stimulate plant systemic resistance. However, the OGS signal patterns and mechanisms of B. cinerea infection in strawberry fruits are still unclear. The current program will analyze the characteristics of cell wall structure and OGS components under B. cinerea infection and clarify the key OGS signal components through exogenous OGS treatments. Transient genetic transformation fruits FAPGIP-BCPG1 and gene knockout mutant BCPG1 will be constructed to compare the cell wall structure and OGS components and reveal the regulation mechanisms of OGS signal generation. The secondary metabolic network mediated by OGs will be analyzed, and the OGs action mode will be explored from the substance metabolism pathway of disease resistance response. Finally, the OGS signal characteristics and mechanisms of interaction between strawberry fruits and B. cinerea will be demonstrated.