Plants utilize a two-tiered immune system consisting of pattern recognition receptor (PRR)-triggered immunity (PTI) and effector-triggered immunity (ETI) to defend themselves against pathogenic microbes. The receptor protein kinase BAK1 plays a central role in multiple PTI signaling pathways in Arabidopsis. However, double mutants made by BAK1 and its closest paralog BKK1 exhibit autoimmune phenotypes, including cell death resembling a typical nucleotide-binding leucine-rich repeat protein (NLR)-mediated ETI response. The molecular mechanisms of the cell death caused by the depletion of BAK1 and BKK1 are poorly understood. Here, we show that the cell-death phenotype of bak1 bkk1 is suppressed when a group of NLRs, ADR1s, are mutated, indicating the cell-death of bak1 bkk1 is the consequence of NLR activation. Furthermore, introduction of a Pseudomonas syringae effector HopB1, which proteolytically cleaves activated BAK1 and its paralogs via either gene transformation or bacterium-delivery, results in a cell-death phenotype in an ADR1s-dependent manner. Our study thus pinpoints that BAK1 and its paralogs are likely guarded by NLRs.

植物利用由模式识别受体（PRR）触发的免疫（PTI）和效应器触发的免疫（ETI）组成的两级免疫系统来防御自身致病微生物。受体蛋白激酶BAK1在拟南芥中的多种PTI信号途径中发挥重要作用。但是，由BAK1及其最接近的同源物BKK1产生的双突变体表现出自身免疫表型，包括类似于典型的核苷酸结合的富含亮氨酸的重复蛋白（NLR）介导的ETI反应的细胞死亡。人们对由BAK1和BKK1耗尽引起的细胞死亡的分子机制了解甚少。在这里，我们显示当一组NLR抑制bak1 bkk1的细胞死亡表型s，ADR1 s发生突变，表明bak1 bkk1的细胞死亡是NLR激活的结果。此外，引入丁香假单胞菌效应器HopB1，其通过基因转化或细菌递送通过蛋白水解方式切割活化的BAK1及其旁系同源物，从而以ADR1 s依赖性方式导致细胞死亡表型。因此，我们的研究指出BAK1及其旁系同源物可能受NLR保护。