Go in for the kill: How plants deploy effector-triggered immunity to combat pathogens

Plant resistance (R) proteins perceive specific pathogen effectors from diverse plant pathogens to initiate defense responses, designated effector-triggered immunity (ETI). Plant R proteins are mostly nucleotide binding-leucine rich repeat (NB-LRR) proteins, which recognize pathogen effectors direct...

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Main Authors: Wu, Liang, Chen, Huan, Curtis, Chad, Fu, Zheng Qing
Format: Online
Language:English
Published: Landes Bioscience 2014
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4189877/
id pubmed-4189877
recordtype oai_dc
spelling pubmed-41898772015-10-01 Go in for the kill: How plants deploy effector-triggered immunity to combat pathogens Wu, Liang Chen, Huan Curtis, Chad Fu, Zheng Qing Review Plant resistance (R) proteins perceive specific pathogen effectors from diverse plant pathogens to initiate defense responses, designated effector-triggered immunity (ETI). Plant R proteins are mostly nucleotide binding-leucine rich repeat (NB-LRR) proteins, which recognize pathogen effectors directly or indirectly through sophisticated mechanisms. Upon activation by effector proteins, R proteins elicit robust defense responses, including a rapid burst of reactive oxygen species (ROS), induced biosynthesis and accumulation of salicylic acid (SA), a rapid programmed cell death (PCD) called hypersensitive response (HR) at the infection sites, and increased expression of pathogenesis-related (PR) genes. Initiation of ETI is correlated with a complex network of defense signaling pathways, resulting in defensive cellular responses and large-scale transcriptional reprogramming events. In this review, we highlight important recent advances on the recognition of effectors, regulation and activation of plant R proteins, dynamic intracellular trafficking of R proteins, induction of cell death, and transcriptional reprogramming associated with ETI. Current knowledge gaps and future research directions are also discussed in this review. Landes Bioscience 2014-10-01 2014-07-10 /pmc/articles/PMC4189877/ /pubmed/25513772 http://dx.doi.org/10.4161/viru.29755 Text en Copyright © 2014 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Wu, Liang
Chen, Huan
Curtis, Chad
Fu, Zheng Qing
spellingShingle Wu, Liang
Chen, Huan
Curtis, Chad
Fu, Zheng Qing
Go in for the kill: How plants deploy effector-triggered immunity to combat pathogens
author_facet Wu, Liang
Chen, Huan
Curtis, Chad
Fu, Zheng Qing
author_sort Wu, Liang
title Go in for the kill: How plants deploy effector-triggered immunity to combat pathogens
title_short Go in for the kill: How plants deploy effector-triggered immunity to combat pathogens
title_full Go in for the kill: How plants deploy effector-triggered immunity to combat pathogens
title_fullStr Go in for the kill: How plants deploy effector-triggered immunity to combat pathogens
title_full_unstemmed Go in for the kill: How plants deploy effector-triggered immunity to combat pathogens
title_sort go in for the kill: how plants deploy effector-triggered immunity to combat pathogens
description Plant resistance (R) proteins perceive specific pathogen effectors from diverse plant pathogens to initiate defense responses, designated effector-triggered immunity (ETI). Plant R proteins are mostly nucleotide binding-leucine rich repeat (NB-LRR) proteins, which recognize pathogen effectors directly or indirectly through sophisticated mechanisms. Upon activation by effector proteins, R proteins elicit robust defense responses, including a rapid burst of reactive oxygen species (ROS), induced biosynthesis and accumulation of salicylic acid (SA), a rapid programmed cell death (PCD) called hypersensitive response (HR) at the infection sites, and increased expression of pathogenesis-related (PR) genes. Initiation of ETI is correlated with a complex network of defense signaling pathways, resulting in defensive cellular responses and large-scale transcriptional reprogramming events. In this review, we highlight important recent advances on the recognition of effectors, regulation and activation of plant R proteins, dynamic intracellular trafficking of R proteins, induction of cell death, and transcriptional reprogramming associated with ETI. Current knowledge gaps and future research directions are also discussed in this review.
publisher Landes Bioscience
publishDate 2014
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4189877/
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