PDF(Pubmed)
Abstract：
Enabling and constraining immune activation is of fundamental importance in maintaining cellular homeostasis. Depleting BAK1 and SERK4, the co-receptors of multiple pattern recognition receptors (PRRs), abolishes pattern-triggered immunity but triggers intracellular NOD-like receptor (NLR)-mediated autoimmunity with an elusive mechanism. By deploying RNAi-based genetic screens in Arabidopsis, we identified BAK-TO-LIFE 2 (BTL2), an uncharacterized receptor kinase, sensing BAK1/SERK4 integrity. BTL2 induces autoimmunity through activating Ca2+ channel CNGC20 in a kinase-dependent manner when BAK1/SERK4 are perturbed. To compensate for BAK1 deficiency, BTL2 complexes with multiple phytocytokine receptors, leading to potent phytocytokine responses mediated by helper NLR ADR1 family immune receptors, suggesting phytocytokine signaling as a molecular link connecting PRR- and NLR-mediated immunity. Remarkably, BAK1 constrains BTL2 activation via specific phosphorylation to maintain cellular integrity. Thus, BTL2 serves as a surveillance rheostat sensing the perturbation of BAK1/SERK4 immune co-receptors in promoting NLR-mediated phytocytokine signaling to ensure plant immunity.
摘要：
启用和限制免疫激活对于维持细胞稳态具有根本重要性。消耗BAK1和SERK4，多种模式识别受体（PRR）的共受体，消除模式触发的免疫，但以难以捉摸的机制触发细胞内NOD样受体（NLR）介导的自身免疫。通过在拟南芥中部署基于RNAi的遗传筛选，我们确定了BAK-TO-LIFE2（BTL2），一种未表征的受体激酶，传感BAK1/SERK4完整性。当BAK1/SERK4被干扰时,BTL2通过以激酶依赖性方式激活Ca2+通道CNGC20诱导自身免疫。为了弥补BAK1缺乏，BTL2与多种植物细胞因子受体的复合物，导致由辅助NLRADR1家族免疫受体介导的有效植物细胞因子应答，表明植物细胞因子信号传导是连接PRR和NLR介导的免疫的分子联系。值得注意的是,BAK1通过特异性磷酸化限制BTL2激活以维持细胞完整性。因此，BTL2充当监测变阻器,感测BAK1/SERK4免疫共受体在促进NLR介导的植物细胞因子信号传导以确保植物免疫中的扰动。
