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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...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5809103/ https://www.ncbi.nlm.nih.gov/pubmed/29385213 http://dx.doi.org/10.1371/journal.ppat.1006878 |
Sumario: | 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. |
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