The Arabidopsis TIR-NBS-LRR protein CSA1 guards BAK1-BIR3 homeostasis and mediates convergence of pattern- and effector-induced immune responses

Arabidopsis BAK1/SERK3, a co-receptor of leucine-rich repeat pattern recognition receptors (PRRs), mediates pattern-triggered immunity (PTI). Genetic inactivation of BAK1 or BAK1-interacting receptor-like kinases (BIRs) causes cell death, but the direct mechanisms leading to such deregulation remains unclear. Here, we found that the TIR-NBS-LRR protein CONSTITUTIVE SHADE AVOIDANCE 1 (CSA1) physically interacts with BIR3, but not with BAK1. CSA1 mediates cell death in bak1-4 and bak1-4 bir3-2 mutants via components of effector-triggered immunity-(ETI) pathways. Effector HopB1-mediated perturbation of BAK1 also results in CSA1-dependent cell death. Likewise, microbial pattern pg23-induced cell death, but not PTI responses, requires CSA1. Thus, we show that CSA1 guards BIR3 BAK1 homeostasis and integrates pattern- and effector-mediated cell death pathways downstream of BAK1. De-repression of CSA1 in the absence of intact BAK1 and BIR3 triggers ETI cell death. This suggests that PTI and ETI pathways are activated downstream of BAK1 for efficient plant immunity. [Display omitted] •BAK1 and BIR3 perturbation is guarded by the TNL CSA1•BAK1 surveillance by CSA1 is required for PRR- and an NLR-receptor-initiated cell death•CSA1 contributes to PTI, but classical PTI responses are not altered in csa1 mutants•Both ETI- and PTI-type defense pathways are activated downstream of BAK1 Schulze, Yu, et al. show that CSA1 mediates cell death initiated by BAK1 inactivation. This cell death is triggered by pattern recognition by cell surface receptors and an effector, recognized by CSA1. Both initiate BAK1 cleavage, indicating that surveillance of BAK1 leads to activation of ETI-type cell death via CSA1.