The Arabidopsis ( Arabidopsis thaliana) FLAGELLIN-SENSING2 (FLS2) is a well-studied RLK and perceives a 22-amino acid epitope of bacterial flagellin called flg22 ( Chinchilla et al., 2006). PTI receptors are receptor-like kinases (RLKs) or receptor-like proteins (RLPs) possessing extracellular ligand-binding domains ( Zipfel, 2014). Although there is significant overlap in PTI- and ETI-based responses, ETI typically induces a stronger response and culminates in programmed cell death at the site of infection ( Chiang and Coaker, 2015). Plants also can recognize specific intracellular pathogen effectors using resistance proteins and induce effector-triggered immunity ( ETI Chiang and Coaker, 2015). A common mechanism for PTI suppression is the secretion of pathogen proteins, called effectors, into the apoplast or inside host cells ( Dou and Zhou, 2012 Sánchez-Vallet et al., 2013). Thus, adapted pathogens must overcome PTI in order to grow and to cause disease. While Ca 2+ influx, the oxidative burst, and MAPK activation occur within minutes of PAMP perception, callose deposition is a later response occurring several hours post perception ( Boller and Felix, 2009). Common PTI responses include Ca 2+ influx, an extracellular reactive oxygen species ( ROS) burst, activation of mitogen-activated protein kinases (MAPKs), transcriptional reprogramming, and callose deposition ( Boller and Felix, 2009). Surface-localized receptors with extracellular domains can perceive conserved pathogen-associated molecular patterns ( PAMPs)/microbe-associated molecular patterns (MAMPs), such as bacterial flagellin or fungal chitin, and induce pattern-triggered immunity ( PTI Zipfel, 2014). There also are large numbers of germline-encoded extracellular and intracellular innate immune receptors that actively perceive pathogens and induce cellular reprogramming for defense ( Zipfel, 2014 Chiang and Coaker, 2015). Plants possess physical barriers to pathogen ingress, including a waxy cuticle and cell wall. Plants are in close contact with a variety of microorganisms, including pathogens. These data support a model where Arabidopsis CRKs are synthesized upon pathogen perception, associate with the FLS2 complex, and coordinately act to enhance plant immune responses. CRK28 self-associated as well as associated with the closely related CRK29. CRK28 associated with BAK1 as well as the activated FLAGELLIN-SENSING2 (FLS2) immune receptor complex. CRK28-mediated cell death required the common receptor-like protein kinase coreceptor BAK1. Expression of CRK28 in Nicotiana benthamiana induced cell death, which required intact extracellular Cys residues and a conserved kinase active site. Enhanced expression of CRK28 in Arabidopsis increased disease resistance to P. In contrast, silencing of multiple bacterial flagellin-induced CRKs resulted in enhanced susceptibility to pathogenic Pseudomonas syringae, indicating functional redundancy in this large gene family. The single transfer DNA insertion lines CRK28 and CRK29, two CRKs induced in response to flagellin perception, did not exhibit robust alterations in immune responses. CRKs possess extracellular Cys-rich domains and constitute a gene family consisting of 46 members in Arabidopsis.
We identified multiple receptor-like protein kinases changing in abundance, including cysteine (Cys)-rich receptor-like kinases (CRKs) that are up-regulated upon the perception of flagellin. We performed quantitative proteomics on plasma membrane-enriched samples from Arabidopsis ( Arabidopsis thaliana) treated with bacterial flagellin. Membrane-localized proteins perceive and respond to biotic and abiotic stresses.
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