Overexpression of the receptor-like kinase BIR1 gene causes SOBIR1- and EDS1-dependent cell death phenotypes 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 Statement Regulation 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.