细菌可以通过接触型分泌系统向相同生境中其他微生物注射效应蛋白，达到抑制竞争者的目的。以往关于效应蛋白的研究主要集中在效应蛋白如何与靶标蛋白互作，抑制竞争者的机制上，然而效应蛋白在细菌自身体内的功能则鲜有报道。与此不同的是，我们发现植物生防产酶溶杆菌OH11 IV型分泌系统效应蛋白Le2361可以抑制真菌的生长，同时Le2361在体内可以与转录因子Clp互作并调控抗真菌代谢物HSAF的合成。Clp可以结合HSAF合成基因的启动子，调控HSAF的合成，并且其结合能力受到小分子信号c-di-GMP的调控。进一步研究发现Le2361可以干扰Clp和c-di-GMP的互作，本项目将分析Le2361调控HSAF合成的关键位点，解析Le2361-Clp蛋白复合物形成的结构基础；探究Le2361通过与Clp互作调控HSAF合成的信号途径。研究结果将有望揭示细菌毒性效应蛋白调控自身生理功能的新机制。

Bacteria inject effectors into other microorganisms in the same habitat through contact dependent secretion system to inhibit competitors. Previous researches on effectors focused on how effectors interact with target protein and inhibit competitors, but functions of effectors in bacteria own cells have not been studied widely. Different from this, we found type IV secretion system effector Le2361 which is secreted by plant bio-control bacterium Lysobacter enzymogenes OH11 may not only inhibit fungal growth, but also regulate biosynthesis of antifungal metabolite HSAF by interacting with transcription factor Clp. Clp regulates HSAF biosynthesis by binding promoter of HSAF biosynthesis genes. The binding affinity of Clp and promoter is regulated by a small molecule signal c-di-GMP. Further study showed that Le2361 regulated HSAF synthesis by inhibiting the interaction of Clp and c-di-GMP. In this project, we will identify the key sites of Le2361 for HSAF biosynthesis regulation, analyze the structural basis for the interaction of Le2361-Clp, and explore signal pathway of HSAF biosynthesis regulation by Le2361. The results of this study will reveal new mechanism on regulation of physiological function in bacteria own cell by toxic effector.