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Survival factor 1 contributes to the oxidative stress response and is required for full virulence of Sclerotinia sclerotiorum
Sclerotinia sclerotiorum is a devastating necrotrophic fungal pathogen that infects over 400 species of plants worldwide. Reactive oxygen species (ROS) modulations are critical for the pathogenic development of S. sclerotiorum. The fungus applies enzymatic and non‐enzymatic antioxidants to cope with...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6589728/ https://www.ncbi.nlm.nih.gov/pubmed/31074170 http://dx.doi.org/10.1111/mpp.12801 |
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author | Yu, Yang Du, Jiao Wang, Yabo Zhang, Mengyao Huang, Zhiqiang Cai, Junsong Fang, Anfei Yang, Yuheng Qing, Ling Bi, Chaowei Cheng, Jiasen |
author_facet | Yu, Yang Du, Jiao Wang, Yabo Zhang, Mengyao Huang, Zhiqiang Cai, Junsong Fang, Anfei Yang, Yuheng Qing, Ling Bi, Chaowei Cheng, Jiasen |
author_sort | Yu, Yang |
collection | PubMed |
description | Sclerotinia sclerotiorum is a devastating necrotrophic fungal pathogen that infects over 400 species of plants worldwide. Reactive oxygen species (ROS) modulations are critical for the pathogenic development of S. sclerotiorum. The fungus applies enzymatic and non‐enzymatic antioxidants to cope with the oxidative stress during the infection processes. Survival factor 1 was identified and characterized to promote survival under conditions of oxidative stress in Saccharomyes cerevisiae. In this research, a gene named SsSvf1 was predicted to encode a survival factor 1 homologue in S. sclerotiorum. SsSvf1 transcripts showed high expression levels in hyphae under oxidative stress. Silencing of SsSvf1 resulted in increased sensitivity to oxidative stress in culture and increased levels of intracellular ROS. Transcripts of SsSvf1 showed a dramatic increase during the initial stage of infection and the gene‐silenced strains displayed reduced virulence on oilseed rape and Arabidopsis thaliana. Inhibition of plant ROS production partially restores virulence of SsSvf1 gene‐silenced strains. SsSvf1 gene‐silenced strains exhibited normal oxalate production, but were impaired in compound appressorium formation and cell wall integrity. The results suggest that SsSvf1 is involved in coping with ROS during fungal‐host interactions and plays a crucial role in the pathogenicity of S. sclerotiorum. |
format | Online Article Text |
id | pubmed-6589728 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-65897282019-09-16 Survival factor 1 contributes to the oxidative stress response and is required for full virulence of Sclerotinia sclerotiorum Yu, Yang Du, Jiao Wang, Yabo Zhang, Mengyao Huang, Zhiqiang Cai, Junsong Fang, Anfei Yang, Yuheng Qing, Ling Bi, Chaowei Cheng, Jiasen Mol Plant Pathol Original Articles Sclerotinia sclerotiorum is a devastating necrotrophic fungal pathogen that infects over 400 species of plants worldwide. Reactive oxygen species (ROS) modulations are critical for the pathogenic development of S. sclerotiorum. The fungus applies enzymatic and non‐enzymatic antioxidants to cope with the oxidative stress during the infection processes. Survival factor 1 was identified and characterized to promote survival under conditions of oxidative stress in Saccharomyes cerevisiae. In this research, a gene named SsSvf1 was predicted to encode a survival factor 1 homologue in S. sclerotiorum. SsSvf1 transcripts showed high expression levels in hyphae under oxidative stress. Silencing of SsSvf1 resulted in increased sensitivity to oxidative stress in culture and increased levels of intracellular ROS. Transcripts of SsSvf1 showed a dramatic increase during the initial stage of infection and the gene‐silenced strains displayed reduced virulence on oilseed rape and Arabidopsis thaliana. Inhibition of plant ROS production partially restores virulence of SsSvf1 gene‐silenced strains. SsSvf1 gene‐silenced strains exhibited normal oxalate production, but were impaired in compound appressorium formation and cell wall integrity. The results suggest that SsSvf1 is involved in coping with ROS during fungal‐host interactions and plays a crucial role in the pathogenicity of S. sclerotiorum. John Wiley and Sons Inc. 2019-05-09 /pmc/articles/PMC6589728/ /pubmed/31074170 http://dx.doi.org/10.1111/mpp.12801 Text en © 2019 The Authors. Molecular Plant Pathology published by British Society for Plant Pathology and John Wiley & Sons Ltd This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Yu, Yang Du, Jiao Wang, Yabo Zhang, Mengyao Huang, Zhiqiang Cai, Junsong Fang, Anfei Yang, Yuheng Qing, Ling Bi, Chaowei Cheng, Jiasen Survival factor 1 contributes to the oxidative stress response and is required for full virulence of Sclerotinia sclerotiorum |
title | Survival factor 1 contributes to the oxidative stress response and is required for full virulence of Sclerotinia sclerotiorum
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title_full | Survival factor 1 contributes to the oxidative stress response and is required for full virulence of Sclerotinia sclerotiorum
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title_fullStr | Survival factor 1 contributes to the oxidative stress response and is required for full virulence of Sclerotinia sclerotiorum
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title_full_unstemmed | Survival factor 1 contributes to the oxidative stress response and is required for full virulence of Sclerotinia sclerotiorum
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title_short | Survival factor 1 contributes to the oxidative stress response and is required for full virulence of Sclerotinia sclerotiorum
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title_sort | survival factor 1 contributes to the oxidative stress response and is required for full virulence of sclerotinia sclerotiorum |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6589728/ https://www.ncbi.nlm.nih.gov/pubmed/31074170 http://dx.doi.org/10.1111/mpp.12801 |
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