title: Activation-Dependent Destruction of a Co-receptor by a Pseudomonas syringae Effector Dampens Plant Immunity.
abstract: The Arabidopsis immune receptor FLS2 and co-receptor BAK1 perceive the bacterial flagellin epitope flg22 to activate plant immunity. To prevent this response, phytopathogenic bacteria deploy a repertoire of effector proteins to perturb immune signaling. However, the effector-induced perturbation is often sensed by the host, triggering another layer of immunity. We report that the Pseudomonas syringae effector HopB1 acts as a protease to cleave immune-activated BAK1. Prior to activation, HopB1 constitutively interacts with FLS2. Upon activation by flg22, BAK1 is recruited to the FLS2-HopB1 complex and is phosphorylated at Thr455. HopB1 then specifically cleaves BAK1 between Arg297 and Gly298 to inhibit FLS2 signaling. Although perturbation of BAK1 is known to trigger increased immune responses in plants, the HopB1-mediated cleavage of BAK1 leads to enhanced virulence, but not disease resistance. This study thus reveals a virulence strategy by which a pathogen effector attacks the plant immune system with minimal host perturbation.
authors.affiliation: State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences (CAS), Beijing 100101, China. Electronic address: lilei2011@genetics.ac.cn.
authors.forename: Lei
authors.initials: L
authors.lastname: Li
authors.affiliation: Center for Plant Science Innovation and School of Biological Sciences, University of Nebraska, Lincoln, NE 68588, USA.
authors.forename: Panya
authors.initials: P
authors.lastname: Kim
authors.affiliation: State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences (CAS), Beijing 100101, China.
authors.forename: Liping
authors.initials: L
authors.lastname: Yu
authors.affiliation: National Institute of Biological Sciences, Beijing 102206, China.
authors.forename: Gaihong
authors.initials: G
authors.lastname: Cai
authors.affiliation: National Institute of Biological Sciences, Beijing 102206, China.
authors.forename: She
authors.initials: S
authors.lastname: Chen
authors.affiliation: Center for Plant Science Innovation and Department of Plant Pathology, University of Nebraska, Lincoln, NE 68588, USA.
authors.forename: James R
authors.initials: JR
authors.lastname: Alfano
authors.affiliation: State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences (CAS), Beijing 100101, China. Electronic address: jmzhou@genetics.ac.cn.
authors.forename: Jian-Min
authors.initials: JM
authors.lastname: Zhou
mesh_terms: D017360:Arabidopsis / Q000276:immunology* / Q000382:microbiology*; D029681:Arabidopsis Proteins / Q000378:metabolism*; D057131:Immune Evasion; D010447:Peptide Hydrolases / Q000378:metabolism*; D057865:Plant Immunity; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*; D059748:Proteolysis; D044224:Pseudomonas syringae / Q000201:enzymology / Q000378:metabolism* / Q000472:pathogenicity*; D037521:Virulence Factors / Q000378:metabolism
chemical_list: D029681:Arabidopsis Proteins; D037521:Virulence Factors; C463660:BAK1 protein, Arabidopsis; D017346:Protein Serine-Threonine Kinases; D010447:Peptide Hydrolases