Open AccessThe fungal pathogen Magnaporthe oryzae suppresses innate immunity by modulating a host potassium channel
Author(s) -
Xuetao Shi,
Yu Long,
Feng He,
Chongyang Zhang,
Ruyi Wang,
Ting Zhang,
Wei Wu,
Zeyun Hao,
Yi Wang,
GuoLiang Wang,
Yuping Ning
Publication year - 2018
Publication title -
plos pathogens
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.719
H-Index - 206
eISSN - 1553-7374
pISSN - 1553-7366
DOI - 10.1371/journal.ppat.1006878
Subject(s) - biology , immunity , effector , innate immune system , plant immunity , pathogen , virulence , magnaporthe , potassium channel , acquired immune system , microbiology and biotechnology , host (biology) , plant disease resistance , immune system , gene , genetics , magnaporthe grisea , oryza sativa , mutant , biophysics , arabidopsis
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.