植物必须精确调控免疫信号转导以防止不必要或长时间免疫激活而损害自身生长发育。MAPK是植物免疫信号转导的中枢。我们前期研究发现拟南芥CDG1，作为激素BR信号转导的正调控因子，在过表达时能显著抑制flg22对MPK3/6和MPK4的激活。CDG1的激酶活性，细胞膜定位以及BR诱导的S234磷酸化均对这种抑制至关重要。flg22能诱导CDG1发生磷酸化。更重要的是，CDG1不仅和flg22受体FLS2有强烈互作，也和已知参与flg22信号转导的MAPKKK——MEKK1互作，以及和丁香假单胞菌效应蛋白AvrPto互作，因而值得深入研究。本项目拟在确认CDG1的负调控功能基础之上，深入研究其负调控的分子机制，探究其与BR拮抗免疫信号转导的关联，并尝试阐明AvrPto与CDG1互作对flg22信号转导的影响。本研究将可能揭示植物免疫信号转导新的负调控机制以及BR拮抗免疫信号转导的新节点。

Plants need to tightly regulate innate immunity to avoid self-damaging due to undesirable or prolonged activation of immunity. MAPKs are crucial signaling hubs in plant innate immunity. Our preliminary data revealed that over-expression of CDG1, a signal transducer in brassinosteriod (BR) signaling, could suppress flg22-induced MPK3/6 and MPK4 activation in Arabidopsis, where its kinase activity, plasma membrane localization and BR-induced Ser234 phosphorylation are all required for such effects. flg22 could trigger CDG1 phosphorylation in vivo. Moreover, CDG1 could strongly interact with the flg22 receptor FLS2 and MEKK1, a known MAPKKK involved in flg22 signaling. Interestingly, CDG1 could also interact with the effector AvrPto from Pseudomonas syringae. Based on these preliminary data, we propose to study the inhibitory role of CDG1 for MAPK activation in Arabidopsis defense signaling, and to thoroughly investigate the molecular mechanisms involved. We also attempt to clarify the relevance between the negative regulation of CDG1 on immune signaling and the antagonism of BR against plant immunity. In addition, we will pinpoint the effect of AvrPto and CDG1 interaction on flg22 signaling. The proposed work has the potential to uncover not only a novel negative regulatory mechanism of plant innate immunity, but also a previously unknown operator of BR antagonism against plant immunity.