The fungal pathogen Magnaporthe oryzae suppresses innate immunity by modulating a host potassium channel.

Potassium (K+) is required by plants for growth and development, and also contributes to immunity against pathogens. However, it has not been established whether pathogens modulate host K+ signaling pathways to enhance virulence and subvert host immunity. Here, we show that the effector protein AvrP...

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Main Authors: Xuetao Shi, Yu Long, Feng He, Chongyang Zhang, Ruyi Wang, Ting Zhang, Wei Wu, Zeyun Hao, Yi Wang, Guo-Liang Wang, Yuese Ning
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2018-01-01
Series:PLoS Pathogens
Online Access:http://europepmc.org/articles/PMC5809103?pdf=render
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spelling doaj-5eec650d0f474677b1bc7d95f36b48b82020-11-25T00:58:00ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742018-01-01141e100687810.1371/journal.ppat.1006878The fungal pathogen Magnaporthe oryzae suppresses innate immunity by modulating a host potassium channel.Xuetao ShiYu LongFeng HeChongyang ZhangRuyi WangTing ZhangWei WuZeyun HaoYi WangGuo-Liang WangYuese NingPotassium (K+) is required by plants for growth and development, and also contributes to immunity against pathogens. However, it has not been established whether pathogens modulate host K+ signaling pathways to enhance virulence and subvert host immunity. Here, we show that the effector protein AvrPiz-t from the rice blast pathogen Magnaporthe oryzae targets a K+ channel to subvert plant immunity. AvrPiz-t interacts with the rice plasma-membrane-localized K+ channel protein OsAKT1 and specifically suppresses the OsAKT1-mediated K+ currents. Genetic and phenotypic analyses show that loss of OsAKT1 leads to decreased K+ content and reduced resistance against M. oryzae. Strikingly, AvrPiz-t interferes with the association of OsAKT1 with its upstream regulator, the cytoplasmic kinase OsCIPK23, which also plays a positive role in K+ absorption and resistance to M. oryzae. Furthermore, we show a direct correlation between blast disease resistance and external K+ status in rice plants. Together, our data present a novel mechanism by which a pathogen suppresses plant host immunity by modulating a host K+ channel.http://europepmc.org/articles/PMC5809103?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Xuetao Shi
Yu Long
Feng He
Chongyang Zhang
Ruyi Wang
Ting Zhang
Wei Wu
Zeyun Hao
Yi Wang
Guo-Liang Wang
Yuese Ning
spellingShingle Xuetao Shi
Yu Long
Feng He
Chongyang Zhang
Ruyi Wang
Ting Zhang
Wei Wu
Zeyun Hao
Yi Wang
Guo-Liang Wang
Yuese Ning
The fungal pathogen Magnaporthe oryzae suppresses innate immunity by modulating a host potassium channel.
PLoS Pathogens
author_facet Xuetao Shi
Yu Long
Feng He
Chongyang Zhang
Ruyi Wang
Ting Zhang
Wei Wu
Zeyun Hao
Yi Wang
Guo-Liang Wang
Yuese Ning
author_sort Xuetao Shi
title The fungal pathogen Magnaporthe oryzae suppresses innate immunity by modulating a host potassium channel.
title_short The fungal pathogen Magnaporthe oryzae suppresses innate immunity by modulating a host potassium channel.
title_full The fungal pathogen Magnaporthe oryzae suppresses innate immunity by modulating a host potassium channel.
title_fullStr The fungal pathogen Magnaporthe oryzae suppresses innate immunity by modulating a host potassium channel.
title_full_unstemmed The fungal pathogen Magnaporthe oryzae suppresses innate immunity by modulating a host potassium channel.
title_sort fungal pathogen magnaporthe oryzae suppresses innate immunity by modulating a host potassium channel.
publisher Public Library of Science (PLoS)
series PLoS Pathogens
issn 1553-7366
1553-7374
publishDate 2018-01-01
description Potassium (K+) is required by plants for growth and development, and also contributes to immunity against pathogens. However, it has not been established whether pathogens modulate host K+ signaling pathways to enhance virulence and subvert host immunity. Here, we show that the effector protein AvrPiz-t from the rice blast pathogen Magnaporthe oryzae targets a K+ channel to subvert plant immunity. AvrPiz-t interacts with the rice plasma-membrane-localized K+ channel protein OsAKT1 and specifically suppresses the OsAKT1-mediated K+ currents. Genetic and phenotypic analyses show that loss of OsAKT1 leads to decreased K+ content and reduced resistance against M. oryzae. Strikingly, AvrPiz-t interferes with the association of OsAKT1 with its upstream regulator, the cytoplasmic kinase OsCIPK23, which also plays a positive role in K+ absorption and resistance to M. oryzae. Furthermore, we show a direct correlation between blast disease resistance and external K+ status in rice plants. Together, our data present a novel mechanism by which a pathogen suppresses plant host immunity by modulating a host K+ channel.
url http://europepmc.org/articles/PMC5809103?pdf=render
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