Loss of the common immune coreceptor BAK1 leads to NLR-dependent cell death

Significance BAK1 plays a key role in multiple PRR-triggered immune signaling pathways. Double mutants generated by BAK1 and its paralog BKK1 show spontaneous cell death, which is not seen in any known PRR mutants. We discovered that the ADR1 class of helper nucleotide-binding leucine-rich repeat proteins (NLRs) is required for the autoimmune responses of bak1 bkk1 . Knocking out three ADR1 s can significantly suppress the cell death of bak1-3 bkk1-1 , suggesting the autoimmune responses of bak1 bkk1 are caused by NLR activation. Furthermore, expression of HopB1, an effector derived from Pseudomonas syringae that cleaves activated BAK1 and its paralogs, leads to cell death similar to bak1 bkk1 , which requires ADR1 s. Our results indicate BAK1 and its paralogs serve as guardees for NLRs.