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

Abstract

The receptor-like kinase BIR1 functions as a negative regulator of cell death and defense in Arabidopsis. Previous studies showed that BIR1 expression is up-regulated during infections with microbes and viruses. However, the biological consequences of BIR1 induction remain unknown. Here, we use a DEX-inducible expression system in Arabidopsis to investigate the outputs associated with physiological and non-physiological levels of BIR1 expression. We show that BIR1 induction at physiological levels significantly interferes with gene expression and plasmodesmata callose deposition triggered by canonical PTI elicitors. We found that plants that accumulated non-physiological doses of BIR1 displayed morphological defects that concur with transcriptomic changes in multiple plant defense genes. We provide experimental evidence that EDS1 and SOBIR1 are required for the ETI-type cell death phenotypes associated to non-physiological levels of BIR1. Here we propose that BIR1 induction may represent a pathogen-triggered mechanism to modulate plant defenses during infection. Our model posits that when BIR1 regulation is lost, BIR1 integrity is sensed by one or several guarding resistance (R) proteins to initiate an ETI-like response, in which SOBIR1 cooperates with EDS1 to transduce signals downstream of R proteins.