AHA1调节气孔免疫的分子机制

气孔由一对保卫细胞组成,在气体交换和蒸腾作用中发挥着重要功能。然而，气孔可以被病原菌所利用，作为病原菌进入植物叶片组织的一个主要途径。植物的气孔会不断地做出反应来阻止病原菌的入侵，相应地，病原菌可以产生一些毒性因子或是分泌一些效应蛋白促进气孔的打开。前期的研究结果表明PM H+-ATPase AHA1可以与免疫信号途径中的RIN4一起发挥作用，AHA1被激活后，引起离子和水的内流，导致气孔的打开。然而AHA1是否可以通过其它途径促进气孔的打开还是未知的。本项目拟在分析AHA1是否可以激活JA的信号通路促进气孔的打开。另外我们初步的研究结果表明效应蛋白AvrX可以通过激活JA的信号通路促进气孔的打开，我们将进一步深入研究效应蛋白AvrX是否通过调节AHA1的活性，来激活JA的信号通路促进气孔的打开，阐明AHA1在调节气孔免疫的分子机制，为深入研究植物和病原菌之间的战争提供重要的依据。

Stomatal pores, formed by a pair of guard cells, function in gas exchange and transpiration. As a natural opening, stomata are exploited by many bacterial pathogens as a gateway for invasion.Successful bacterial pathogens have evolved various virulence factors to re-open stomata..Recent data indicate that PM H+-ATPase working with RIN4 regulate stomatal openning during bacterial invasion by causing swelling of the guard cells. However, it is not clear whether this process is linked to JA signaling.In this program, we will analyze whether AHA1 can activate JA signaling to open stomata. Furthermore, our preliminary results show that AvrX can activate JA signaling to open stomata, whether AvrX manipulates AHA1 activity to activate JA signaling,causing stomatal openning will be studied. This project will reveal the interactions between plant and pathogen in stomatal immunity and provide great insights into the regulation mechanism of stomatal immunity.