Open AccessSurvival factor 1 contributes to the oxidative stress response and is required for full virulence of Sclerotinia sclerotiorum
Author(s) -
Yu Yang,
Du Jiao,
Wang Yabo,
Zhang Mengyao,
Huang Zhiqiang,
Cai Junsong,
Fang Anfei,
Yang Yuheng,
Qing Ling,
Bi Chaowei,
Cheng Jiasen
Publication year - 2019
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/mpp.12801
Subject(s) - sclerotinia sclerotiorum , biology , oxidative stress , microbiology and biotechnology , virulence , gene silencing , reactive oxygen species , gene , sclerotinia , arabidopsis thaliana , fungus , genetics , botany , mutant , biochemistry
Summary 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 .