Overexpression of the Receptor-Like Kinase BIR1 Causes SOBIR1- and EDS1-Dependent Cell Death Phenotypes in Arabidopsis.

Abstract

The receptor-like kinase BAK1-INTERACTING RECEPTOR-LIKE KINASE 1 (BIR1) negatively regulates multiple resistance signalling pathways in Arabidopsis thaliana. Previous studies showed that loss of BIR1 function causes extensive cell death and constitutive activation of immune responses. Using a dexamethasone (DEX)-inducible system, we investigated the effects of BIR1 overexpression on plant development and immunity. Overexpression of BIR1, in the absence of microbes or elicitors, led to cell death phenotypes that resembled the effects of BIR1 depletion in knockout plants. We also observed transcriptional outputs that greatly overlap with canonical pathogen-triggered immunity and effector-triggered immunity (ETI), suggesting that BIR1 modulates immune responses by influencing both pathways. To investigate the genetic basis of BIR1 phenotypes, we conditionally expressed BIR1 in various Arabidopsis immune mutants including sobir1, bak1, eds1, sid2 and eds5. We found that ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1) and SUPPRESSOR OF BIR1-1 (SOBIR1) are necessary for ETI-type cell death seen with BIR1 overexpression. These results support the hypothesis that an excess of BIR1 may be detected by guarding NLR proteins, triggering a cell death response in which SOBIR1 and EDS1 cooperate to transduce signals downstream of R proteins.