Date Published: August 5, 2016
Publisher: Public Library of Science
Author(s): Daniel Couto, Roda Niebergall, Xiangxiu Liang, Christoph A. Bücherl, Jan Sklenar, Alberto P. Macho, Vardis Ntoukakis, Paul Derbyshire, Denise Altenbach, Dan Maclean, Silke Robatzek, Joachim Uhrig, Frank Menke, Jian-Min Zhou, Cyril Zipfel, Libo Shan.
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.
Recognition of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors (PRRs) initiates a complex signalling cascade leading to PRR-triggered immunity (PTI) [1, 2]. In plants, PRRs are plasma membrane (PM)-localized receptor kinases (RKs) or receptor-like proteins (RLPs) . These PRRs typically form dynamic complexes with other regulatory RKs to initiate immune signalling [4, 5]. The Arabidopsis thaliana (hereafter Arabidopsis) leucine-rich repeat (LRR)-RKs FLS2 and EFR, which respectively recognize the bacterial PAMPs flagellin (or the epitope flg22) and EF-Tu (or the epitope elf18), are amongst the best-studied plant PRRs [6, 7]. Upon ligand binding, FLS2 and EFR rapidly form a heteromeric complex with the LRR-RK BAK1/SERK3 resulting in the phosphorylation of both RKs [8–13]. This initiates a series of downstream responses, such as changes in ion fluxes, reactive oxygen species (ROS) production, activation of mitogen-activated protein kinase (MAPK) cascades, transcriptional reprogramming, callose deposition, and finally immunity against microbial pathogens .
Appropriate initiation, timing and amplitude of immune signalling must be carefully regulated to avoid excessive or nonspecific activation of immune responses, which can lead to autoimmune and inflammatory diseases [49, 50]. The mechanisms and pathways that negatively regulate PRR-triggered immunity (PTI) in mammals have been extensively characterized [49, 51, 52]. However, much less is known in plants, where a fine balance between immunity and growth is important for their optimal reproductive success [53, 54].