异三聚体G蛋白（Gα，Gβ和Gγ）是动植物细胞响应外界刺激的信号转导中枢。Gα是异三聚体G蛋白激活的关键，但目前主流观点认为拟南芥Gα（GPA1）不参与天生免疫。我们前期研究发现gpa1突变体有诸多响应细菌鞭毛（flg22）的信号转导缺陷。利用原生质体和免疫共沉淀技术，我们发现一条FLS2（鞭毛受体）－BAK1（共受体）－RGS1（Gα抑制蛋白）－GPA1信号转导通路，调控鞭毛诱导下G蛋白从受体复合物的解离，以避免胞吞和降解。GPA1能与RbohD互作，并以BIK1非依赖的方式调控flg22诱导的ROS爆发。有趣的是，flg22激活的Gα保持与Gβ互作，该发现很可能修正现有的植物G蛋白工作模型。本项目拟在确认上述发现的基础上，阐明flg22激活GPA1以及GPA1调控RbohD活性的分子机制。本研究将可能改变GPA1不参与天生免疫的现有观点，并揭示植物Gα正调控天生免疫信号转导的新机制。

Heterotrimeric G proteins composed of Gα，Gβ and Gγ are pivotal signaling modules in plant and animal cells in response to diverse extracellular stimuli. Gα is the key for heterotrimeric G protein activation. However, it is widely thought that Arabidopsis Ga (GPA1) is not involved in innate immunity. Our preliminary data showed that the gpa1 mutant exhibits multiple immunodeficiencies in response to flg22, an eliciting epitope of bacterial flagellin. By protoplast-based co-IP assays, we uncovered a previously unknown signaling pathway consisting of the flg22 receptor FLS2, co-receptor BAK1, Gα's inhibitor RGS1 and GPA1. This pathway regulates flg22-induced dissociation of the G protein complex from the receptor complex, presumably to avoid flg22-induced co-endocytosis and degradation. GPA1 is able to interact with the NADPH oxidase RbohD, regulating flg22-induced ROS burst in a BIK1-independent manner. Interestingly, flg22-activated Gα retains the interaction with Gβ, challenging the current working model of plant G proteins that Gα and Gβ separate upon activation. Based on these preliminary data, we attempt to further clarify the molecular mechanisms how GPA1 is activated by flg22 and how GPA1 affects the activity of RbohD regarding flg22-induced ROS burst. The proposed work may overturn the dogma that GPA1 is irrelevant to Arabidopsis immunity and reveal a positive regulatory role of Ga on plant immune signaling.