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

Author:

Guzmán-Benito IreneORCID,Robinson Carmen,Hua ChenleiORCID,Sede Ana RocioORCID,Elvira-González LauraORCID,Punzón Isabel,Heinlein Manfred,Nürnberger ThorstenORCID,Llave César

Abstract

SummaryThe receptor-like kinase BAK1-INTERACTING RECEPTOR-LIKE KINASE 1 (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 dexamethasone (DEX)-inducible expression system inArabidopsis thalianato 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 pattern-triggered immunity (PTI) elicitors. 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 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 non-physiological levels of BIR1We propose that BIR1 induction may represent a pathogen-triggered mechanism to modulate plant defenses during infection. Our model predicts 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.

Publisher

Cold Spring Harbor Laboratory

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