植物在与微生物无止境的相互较量中进化形成了复杂精细的防御策略避免病害的发生。对病原微生物的识别防御经常会导致植物细胞程序死亡超敏反应，通过同时杀死病原菌和感染宿主细胞限制病原的定植扩散。由于这种防御反应在植物免疫中的重要作用，它可能成为病原攻击和植物调控的靶标。近年来在植物免疫启动过程已取得较多进展，但对于如何关闭免疫应答，尤其是细胞死亡超敏反应尚不清楚。本项目中，番茄LeSL1具有E3泛素连接酶活性，对多个R蛋白介导免疫反应均有很强抑制作用。同时，LeSL1还与病原菌P. syringae pv tomato效应蛋白AvrPtoB直接互作。LeSL1是否被病原菌“劫持”利用，或在病原菌存在时被植物作为“陷阱”，以及LeSL1的调控靶标，均有待深入研究。因此，本工作将解析番茄E3连接酶LeSL1的免疫调控功能，进一步阐释植物防御-生长状态转换、病原微生物-植物相互作用分子机制。

Along with the endless process of interplay between plants and microbial pathogens, plants have evolved elaborate defense strategies to prevent diseases caused by pathogens they encounter. Recognition and resistance to pathogen often results in hypersensitive response-based programmed cell death, which limits pathogen establishment and spread by killing both pathogen and infected host cell. Given the important role of this defense reaction in plant immunity, it has potential as a target for pathogen attack and plant regulation. Considerable breakthroughs have recently been made on triggerring of plant immunity. However, the mechanisms underlying the down regulation of the defense, especially hypersensitive response-based programmed cell death, still remain unknown. In the present work, tomato LeSL1, which possesses E3 ubiquitin ligase activity, is found to strongly repress diverse R proteins mediated hypersensitive reaction. Meanwhile, LeSL1 interacts with AvrPtoB, an effector protein of pathogen P. syringae pv tomoto. Whether LeSL1 is hijacked by pathogen or works as a plant trap after pathogen recognition, and the regulated target proteins by LeSL1 need thorough investigations. In this study, multidisciplinary techniques are going to be employed to unravel the immune regulation function of tomato E3 ligase LeSL1 to further illustrate the molecular mechanisms on plant defense-growth transition and plant-pathogen interaction.