The receptor-like kinase BIR1 inhibits elicitor-induced plasmodesmata callose deposition and PTI gene expression and requires EDS1 and SOBIR1 to cause dose-dependent cell-death in Arabidopsis
The receptor-like kinase BAK1-INTERACTING RECEPTOR-LIKE KINASE 1 (BIR1) functions as a negative regulator of multiple resistance signaling pathways in Arabidopsis thaliana. Previous studies showed that loss of BIR1 function leads to extensive cell death and activation of constitutive immune responses. Here, we use a dexamethasone (DEX)-inducible expression system to investigate the impact of BIR1 overexpression on plant growth and development and immune regulation. We show that, in the absence of microbes or microbe-derived elicitors/effectors, plants that overexpress BIR1 displayed cell death phenotypes that concur with the transcriptomic up-regulation of multiple immune pathways involved in pathogen perception and defense signal transduction. BIR1 overexpression has similar loss-of-function effects to BIR1 depletion in knockout plants, which suggests that proper BIR1 homeostasis requires a tight regulation of BIR1 expression within a functional threshold. We show that ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1) and SUPPRESSOR OF BIR1-1 (SOBIR1) are required for the effector-triggered immunity (ETI)-type cell death phenotypes associated with overexpression of BIR1. Our data is then consistent with the current hypothesis by which loss of BIR1 regulation and/or integrity is sensed by one or several guarding resistance (NLR) proteins to initiate a cell death response, in which SOBIR1 cooperates with EDS1 to transduce signals downstream of R proteins. Summary StatementRegulation of the receptor-like kinase BIR1 has a strong impact on plant growth and development and immune homeostasis in Arabidopsis. BIR1 overexpression causes cell death-and senescence-like phenotypes that require EDS1 and SOBIR1 signaling pathways, and that resemble to those observed by BIR1 depletion.