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

PLoS Pathog. 2018 Jan 31;14(1):e1006878. doi: 10.1371/journal.ppat.1006878. eCollection 2018 Jan.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Host-Pathogen Interactions / genetics
  • Host-Pathogen Interactions / immunology
  • Immune Evasion* / genetics
  • Immunity, Innate / genetics
  • Magnaporthe / pathogenicity
  • Magnaporthe / physiology*
  • Organisms, Genetically Modified
  • Oryza / genetics
  • Oryza / immunology
  • Oryza / microbiology*
  • Plant Diseases / genetics
  • Plant Diseases / immunology
  • Plant Diseases / microbiology
  • Plants, Genetically Modified
  • Potassium Channels / genetics*
  • Potassium Channels / metabolism
  • Virulence / genetics

Substances

  • Potassium Channels

Grants and funding

This project was supported by grants from the National Key Research and Development Program of China (http://program.most.gov.cn/) (2016YFD0100600 to YN), the National Natural Science Foundation of China (http://www.nsfc.gov.cn/) (31571944 to YN and 31622008 to YW), the Young Elite Scientist Sponsorship of China Association for Science and Technology (http://www.cast.org.cn/) (2015QNRC001 to YN), and the US National Science Foundation (IOS#1120949 to GLW). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.