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The GYF domain protein PSIG1 dampens the induction of cell death during plant-pathogen interactions
The induction of rapid cell death is an effective strategy for plants to restrict biotrophic and hemi-biotrophic pathogens at the infection site. However, activation of cell death comes at a high cost, as dead cells will no longer be available for defense responses nor general metabolic processes. I...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5657617/ https://www.ncbi.nlm.nih.gov/pubmed/29073135 http://dx.doi.org/10.1371/journal.pgen.1007037 |
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author | Matsui, Hidenori Nomura, Yuko Egusa, Mayumi Hamada, Takahiro Hyon, Gang-Su Kaminaka, Hironori Watanabe, Yuichiro Ueda, Takashi Trujillo, Marco Shirasu, Ken Nakagami, Hirofumi |
author_facet | Matsui, Hidenori Nomura, Yuko Egusa, Mayumi Hamada, Takahiro Hyon, Gang-Su Kaminaka, Hironori Watanabe, Yuichiro Ueda, Takashi Trujillo, Marco Shirasu, Ken Nakagami, Hirofumi |
author_sort | Matsui, Hidenori |
collection | PubMed |
description | The induction of rapid cell death is an effective strategy for plants to restrict biotrophic and hemi-biotrophic pathogens at the infection site. However, activation of cell death comes at a high cost, as dead cells will no longer be available for defense responses nor general metabolic processes. In addition, necrotrophic pathogens that thrive on dead tissue, take advantage of cell death-triggering mechanisms. Mechanisms by which plants solve this conundrum remain described. Here, we identify PLANT SMY2-TYPE ILE-GYF DOMAIN-CONTAINING PROTEIN 1 (PSIG1) and show that PSIG1 helps to restrict cell death induction during pathogen infection. Inactivation of PSIG1 does not result in spontaneous lesions, and enhanced cell death in psig1 mutants is independent of salicylic acid (SA) biosynthesis or reactive oxygen species (ROS) production. Moreover, PSIG1 interacts with SMG7, which plays a role in nonsense-mediated RNA decay (NMD), and the smg7-4 mutant allele mimics the cell death phenotype of the psig1 mutants. Intriguingly, the psig1 mutants display enhanced susceptibility to the hemi-biotrophic bacterial pathogen. These findings point to the existence and importance of the SA- and ROS-independent cell death constraining mechanism as a part of the plant immune system. |
format | Online Article Text |
id | pubmed-5657617 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-56576172017-11-09 The GYF domain protein PSIG1 dampens the induction of cell death during plant-pathogen interactions Matsui, Hidenori Nomura, Yuko Egusa, Mayumi Hamada, Takahiro Hyon, Gang-Su Kaminaka, Hironori Watanabe, Yuichiro Ueda, Takashi Trujillo, Marco Shirasu, Ken Nakagami, Hirofumi PLoS Genet Research Article The induction of rapid cell death is an effective strategy for plants to restrict biotrophic and hemi-biotrophic pathogens at the infection site. However, activation of cell death comes at a high cost, as dead cells will no longer be available for defense responses nor general metabolic processes. In addition, necrotrophic pathogens that thrive on dead tissue, take advantage of cell death-triggering mechanisms. Mechanisms by which plants solve this conundrum remain described. Here, we identify PLANT SMY2-TYPE ILE-GYF DOMAIN-CONTAINING PROTEIN 1 (PSIG1) and show that PSIG1 helps to restrict cell death induction during pathogen infection. Inactivation of PSIG1 does not result in spontaneous lesions, and enhanced cell death in psig1 mutants is independent of salicylic acid (SA) biosynthesis or reactive oxygen species (ROS) production. Moreover, PSIG1 interacts with SMG7, which plays a role in nonsense-mediated RNA decay (NMD), and the smg7-4 mutant allele mimics the cell death phenotype of the psig1 mutants. Intriguingly, the psig1 mutants display enhanced susceptibility to the hemi-biotrophic bacterial pathogen. These findings point to the existence and importance of the SA- and ROS-independent cell death constraining mechanism as a part of the plant immune system. Public Library of Science 2017-10-26 /pmc/articles/PMC5657617/ /pubmed/29073135 http://dx.doi.org/10.1371/journal.pgen.1007037 Text en © 2017 Matsui et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Matsui, Hidenori Nomura, Yuko Egusa, Mayumi Hamada, Takahiro Hyon, Gang-Su Kaminaka, Hironori Watanabe, Yuichiro Ueda, Takashi Trujillo, Marco Shirasu, Ken Nakagami, Hirofumi The GYF domain protein PSIG1 dampens the induction of cell death during plant-pathogen interactions |
title | The GYF domain protein PSIG1 dampens the induction of cell death during plant-pathogen interactions |
title_full | The GYF domain protein PSIG1 dampens the induction of cell death during plant-pathogen interactions |
title_fullStr | The GYF domain protein PSIG1 dampens the induction of cell death during plant-pathogen interactions |
title_full_unstemmed | The GYF domain protein PSIG1 dampens the induction of cell death during plant-pathogen interactions |
title_short | The GYF domain protein PSIG1 dampens the induction of cell death during plant-pathogen interactions |
title_sort | gyf domain protein psig1 dampens the induction of cell death during plant-pathogen interactions |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5657617/ https://www.ncbi.nlm.nih.gov/pubmed/29073135 http://dx.doi.org/10.1371/journal.pgen.1007037 |
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