Abstract

Pathogen-associated molecular pattern (PAMP)-trigged immunity (PTI) is the first defensive line of plant innate immunity and is mediated by pattern recognition receptors. Here, we show that a mutation in BR-SIGNALING KINASE1 (BSK1), a substrate of the brassinosteroid (BR) receptor BRASSINOSTEROID INSENSITIVE1, suppressed the powdery mildew resistance caused by a mutation inENHANCED DISEASE RESISTANCE2, which negatively regulates powdery mildew resistance and programmed cell death, inArabidopsis thaliana. A loss-of-functionbsk1mutant displayed enhanced susceptibility to virulent and avirulent pathogens, includingGolovinomyces cichoracearum,Pseudomonas syringae, andHyaloperonospora arabidopsidis. Thebsk1mutant also accumulated lower levels of salicylic acid upon infection withG. cichoracearumandP. syringae. BSK1 belongs to a receptor-like cytoplasmic kinase family and displays kinase activity in vitro; this kinase activity is required for its function. BSK1 physically associates with thePAMPreceptor FLAGELLIN SENSING2 and is required for a subset of flg22-induced responses, including the reactive oxygen burst, but not for mitogen-activated protein kinase activation. Our data demonstrate that BSK1 is involved in positive regulation ofPTI. Together with previous findings, our work indicates that BSK1 represents a key component directly involved in bothBRsignaling and plant immunity.