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The Leucine-Rich Repeat Receptor Kinase BIR2 Is a Negative Regulator of BAK1 in Plant Immunity
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
 
ID 2367453
Author(s) Halter, Thierry; Imkampe, Julia; Mazzotta, Sara; Wierzba, Michael; Postel, Sandra; Bücherl, Christoph; Kiefer, Christian; Stahl, Mark; Chinchilla, Delphine; Wang, Xiaofeng; Nürnberger, Thorsten; Zipfel, Cyril; Clouse, Steven; Borst, Jan Willem; Boeren, Sjef; de Vries, Sacco C; Tax, Frans; Kemmerling, Birgit
Author(s) at UniBasel Chinchilla, Delphine
Year 2014
Title The Leucine-Rich Repeat Receptor Kinase BIR2 Is a Negative Regulator of BAK1 in Plant Immunity
Journal Current biology
Volume 24
Number 2
Pages / Article-Number 134-43
Abstract

Transmembrane leucine-rich repeat (LRR) receptors are commonly used innate immune receptors in plants and animals but can also sense endogenous signals to regulate development. BAK1 is a plant LRR-receptor-like kinase (RLK) that interacts with several ligand-binding LRR-RLKs to positively regulate their functions. BAK1 is involved in brassinosteroid-dependent growth and development, innate immunity, and cell-death control by interacting with the brassinosteroid receptor BRI1, immune receptors, such as FLS2 and EFR, and the small receptor kinase BIR1, respectively.; Identification of in vivo BAK1 complex partners by LC/ESI-MS/MS uncovered two novel BAK1-interacting RLKs, BIR2 and BIR3. Phosphorylation studies revealed that BIR2 is unidirectionally phosphorylated by BAK1 and that the interaction between BAK1 and BIR2 is kinase-activity dependent. Functional analyses of bir2 mutants show differential impact on BAK1-regulated processes, such as hyperresponsiveness to pathogen-associated molecular patterns (PAMP), enhanced cell death, and resistance to bacterial pathogens, but have no effect on brassinosteroid-regulated growth. BIR2 interacts constitutively with BAK1, thereby preventing interaction with the ligand-binding LRR-RLK FLS2. PAMP perception leads to BIR2 release from the BAK1 complex and enables the recruitment of BAK1 into the FLS2 complex.; Our results provide evidence for a new regulatory mechanism for innate immune receptors with BIR2 acting as a negative regulator of PAMP-triggered immunity by limiting BAK1-receptor complex formation in the absence of ligands.

Publisher Cell Press
ISSN/ISBN 0960-9822
edoc-URL http://edoc.unibas.ch/dok/A6223570
Full Text on edoc No
Digital Object Identifier DOI 10.1016/j.cub.2013.11.047
PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/24388849
ISI-Number WOS:000329944400019
Document type (ISI) Journal Article
 
   

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29/03/2024