title: BIK1 interacts with PEPRs to mediate ethylene-induced immunity.
abstract: Plants have evolved intricate immune mechanisms to combat pathogen infection. Upon perception of pathogen-derived signals, plants accumulate defense hormones such as ethylene (ET), jasmonate, salicylate, and damage-associated molecular patterns to amplify immune responses. In particular, the Arabidopsis peptide Pep1 and its family members are thought to be damage-associated molecular patterns that trigger immunity through Pep1 receptor kinases PEPR1 and PEPR2. Here we show that PEPR1 specifically interacts with receptor-like cytoplasmic kinases botrytis-induced kinase 1 (BIK1) and PBS1-like 1 (PBL1) to mediate Pep1-induced defenses. In vitro and in vivo studies suggested that PEPR1, and likely PEPR2, directly phosphorylates BIK1 in response to Pep1 treatment. Surprisingly, the pepr1/pepr2 double-mutant seedlings displayed reduced in sensitivity to ET, as indicated by the elongated hypocotyls. ET-induced expression of defense genes and resistance to Botrytis cinerea were compromised in pepr1/pepr2 and bik1 mutants, reenforcing an important role of PEPRs and BIK1 in ET-mediated defense signaling. Pep treatment partially mimicked ET-induced seedling growth inhibition in a PEPR- and BIK1-dependent manner. Furthermore, both ET and Pep1 treatments induced BIK1 phosphorylation in a PEPR-dependent manner. However, the Pep1-induced BIK1 phosphorylation, seedling growth inhibition, and defense gene expression were independent of canonical ET signaling components. Together our results illustrate a mechanism by which ET and PEPR signaling pathways act in concert to amplify immune responses.
authors: School of Life Science, Nanjing University, Nanjing 210093, China.
authors: Zixu
authors: Z
authors: Liu
authors: Ying
authors: Y
authors: Wu
authors: Fan
authors: F
authors: Yang
authors: Yiyue
authors: Y
authors: Zhang
authors: She
authors: S
authors: Chen
authors: Qi
authors: Q
authors: Xie
authors: Xingjun
authors: X
authors: Tian
authors: Jian-Min
authors: JM
authors: Zhou
mesh_terms: D017360:Arabidopsis / Q000276:immunology*; D029681:Arabidopsis Proteins / Q000378:metabolism*; D018076:DNA, Complementary / Q000378:metabolism; D060467:Disease Resistance; D005030:Ethylenes / Q000494:pharmacology*; D017930:Genes, Reporter; D009154:Mutation; D010766:Phosphorylation; D010937:Plant Growth Regulators / Q000494:pharmacology; D057865:Plant Immunity; D054730:Protein Interaction Domains and Motifs; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*; D011956:Receptors, Cell Surface / Q000378:metabolism*; D016897:Respiratory Burst; D015398:Signal Transduction; D020798:Two-Hybrid System Techniques
chemical_list: D029681:Arabidopsis Proteins; D018076:DNA, Complementary; D005030:Ethylenes; C512592:PEPR1 protein, Arabidopsis; D010937:Plant Growth Regulators; D011956:Receptors, Cell Surface; C036216:ethylene; C509522:BIK1 protein, Arabidopsis; C582179:PEPR2 protein, Arabidopsis; D017346:Protein Serine-Threonine Kinases