Abstract
Arabidopsis thaliana BOTRYTIS-INDUCED KINASE1 (BIK1) regulates immune responses to a distinct class of pathogens. Here, mechanisms underlying BIK1 function and its interactions with other immune response regulators were determined. We describe BIK1 function as a component of ethylene (ET) signaling and PAMP-triggered immunity (PTI) to fungal pathogens. BIK1 in vivo kinase activity increases in response to flagellin peptide (flg22) and the ET precursor 1-aminocyclopropane-1-carboxylic acid (ACC) but is blocked by inhibition of ET perception. BIK1 induction by flg22, ACC, and pathogens is strictly dependent on EIN3, and the bik1 mutation results in altered expression of ET-regulated genes. BIK1 site-directed mutants were used to determine residues essential for phosphorylation and biological functions in planta, including PTI, ET signaling, and plant growth. Genetic analysis revealed flg22-induced PTI to Botrytis cinerea requires BIK1, EIN2, and HUB1 but not genes involved in salicylate (SA) functions. BIK1-mediated PTI to Pseudomonas syringae is modulated by SA, ET, and jasmonate signaling. The coi1 mutation suppressed several bik1 phenotypes, suggesting that COI1 may act as a repressor of BIK1 function. Thus, common and distinct mechanisms underlying BIK1 function in mediating responses to distinct pathogens are uncovered. In sum, the critical role of BIK1 in plant immune responses hinges upon phosphorylation, its function in ET signaling, and complex interactions with other immune response regulators.
Highlights
Mechanisms of plant defense against microbial infection have been studied extensively and the major immune response pathways identified along with many of their genetic components
We demonstrate the biochemical, molecular, and genetic bases of BOTRYTIS-INDUCED KINASE1 (BIK1) function in pathogenassociated molecular patterns (PAMPs)-triggered immunity (PTI) to the necrotrophic fungus B. cinerea and the hemibiotrophic bacterial pathogen Pst, extending our previous observations into the mechanisms underlying the role of BIK1 as an immune response regulator
In vitro and in vivo biochemical assays using BIK1 site-directed mutants identified BIK1 residues contributing to BIK1 and transphosphorylation as well as their biological roles in ET and PTI responses
Summary
Mechanisms of plant defense against microbial infection have been studied extensively and the major immune response pathways identified along with many of their genetic components. Recognition of microbial effectors activates a highly specific and efficient form of plant defense known as effector-triggered immunity (ETI) (Jones and Dangl, 2006). Recognition of PAMPs or effectors is mediated by diverse plant proteins that confer specificity in the activation of immune responses. Effector recognition is mediated by R proteins, which have been widely studied and predominantly consist of nucleotide binding site–leucine-rich repeat proteins and include receptor-like kinases (RLKs). RLKs, such as the chitin receptor LysM/CERK1, the flagellin receptor FLS2, and the receptor for bacterial EF-TU EFR1, have been identified as critical early determinants of PTI (Gomez-Gomez and Boller, 2000; Zipfel et al, 2006; Miya et al, 2007).
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