小背景：The receptor protein kinase BAK1 plays a central role in multiple PTI signaling pathways in Arabidopsis.

研究基础：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.

提出问题：The molecular mechanisms of the cell death caused by the depletion of BAK1 and BKK1 are poorly understood.

结果1：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.

结果2：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.

结论：Our study thus pinpoints that BAK1 and its paralogs are likely guarded by NLRs.