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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Landes Bioscience
2014
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Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4189877/ |
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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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1613142072532926464 |