The Arabidopsis Protein Phosphatase PP2C38 Negatively Regulates the Central Immune Kinase BIK1

被引：7

作者：

Couto, Daniel ^{[1
]}

Niebergall, Roda ^{[1
,5
]}

Liang, Xiangxiu ^{[2
]}

Bucherl, Christoph A. ^{[1
]}

Sklenar, Jan ^{[1
]}

Macho, Alberto P. ^{[1
,6
]}

Ntoukakis, Vardis ^{[1
,7
]}

Derbyshire, Paul ^{[1
]}

Altenbach, Denise ^{[3
,8
]}

Maclean, Dan ^{[1
]}

Robatzek, Silke ^{[1
,3
]}

Uhrig, Joachim ^{[4
,9
]}

Menke, Frank ^{[1
]}

Zhou, Jian-Min ^{[2
]}

Zipfel, Cyril ^{[1
]}

机构：

[1] Sainsbury Lab, Norwich Res Pk, Norwich, Norfolk, England

[2] Chinese Acad Sci, Inst Genet & Dev Biol, Beijing, Peoples R China

[3] Max Planck Inst Plant Breeding Res, Cologne, Germany

[4] Univ Cologne, Bot Inst 3, Cologne, Germany

[5] Univ Munster, Fac Biol, Munster, Germany

[6] Chinese Acad Sci, Shanghai Ctr Plant Stress Biol, Shanghai, Peoples R China

[7] Univ Warwick, Sch Life Sci, Coventry, W Midlands, England

[8] BIOREBA AG, Reinach, Switzerland

[9] Univ Gottingen, Schwann Schleiden Forschungszentrum Mol Zellbiol, Gottingen, Germany

来源：

PLOS PATHOGENS | 2016年 / 12卷 / 08期

基金：

欧洲研究理事会;

关键词：

NADPH OXIDASE RBOHD; PLANT INNATE IMMUNITY; CYTOPLASMIC KINASE; PSEUDOMONAS-SYRINGAE; RECEPTOR COMPLEXES; TRIGGERED IMMUNITY; ACTIVATION; BAK1; PERCEPTION; GROWTH;

D O I：

10.1371/journal.ppat.1005811

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Plants recognize pathogen-associated molecular patterns (PAMPs) via cell surface-localized pattern recognition receptors (PRRs), leading to PRR-triggered immunity (PTI). The Arabidopsis cytoplasmic kinase BIK1 is a downstream substrate of several PRR complexes. How plant PTI is negatively regulated is not fully understood. Here, we identify the protein phosphatase PP2C38 as a negative regulator of BIK1 activity and BIK1-mediated immunity. PP2C38 dynamically associates with BIK1, as well as with the PRRs FLS2 and EFR, but not with the co-receptor BAK1. PP2C38 regulates PAMP-induced BIK1 phosphorylation and impairs the phosphorylation of the NADPH oxidase RBOHD by BIK1, leading to reduced oxidative burst and stomatal immunity. Upon PAMP perception, PP2C38 is phosphorylated on serine 77 and dissociates from the FLS2/EFR-BIK1 complexes, enabling full BIK1 activation. Together with our recent work on the control of BIK1 turnover, this study reveals another important regulatory mechanism of this central immune component.

引用

页数：24

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