Both Light-Induced SA Accumulation and ETI Mediators Contribute to the Cell Death Regulated by and

Receptor-like kinases BAK1 and BKK1 modulate multiple cellular processes including brassinosteroid signaling and PRR-mediated PTI in Arabidopsis. Our previous reports also demonstrated that double mutants exhibit a spontaneous cell death phenotype under normal growth condition. With an unknown mechanism, the cell death in is significantly suppressed when grown in dark but can be quickly induced by light. Furthermore, little is known about intrinsic components involved in and -regulated cell death pathway. In this study, we analyzed how light functions as an initiator of cell death and identified ETI components to act as mediators of cell death signaling in . Cell death suppressed in by growing in dark condition recurred upon exogenously treated SA. SA biosynthesis-related genes and , which encode chloroplast-localized proteins, were highly expressed in . When crossed to or was capable of efficiently suppressing the cell death. It suggested that overly produced SA is crucial for inducing cell death in grown in light. Notably, or single mutant was shown to be more susceptible but double mutant exhibited enhanced resistance to bacterial pathogen, suggesting immune signaling other than PTI is activated in . Moreover, genetic analyses showed that mutation in or , key ETI mediator, significantly suppressed the cell death in . In this study, we revealed that light-triggered SA accumulation plays major role in inducing the cell death in , mediated by ETI components.