Survival factor 1 contributes to the oxidative stress response and is required for full virulence of Sclerotinia sclerotiorum. (9th May 2019)

• Record Type: Journal Article
• Authors: Yu, Yang; Du, Jiao; Wang, Yabo; Zhang, Mengyao; Huang, Zhiqiang; Cai, Junsong; Fang, Anfei; Yang, Yuheng; Qing, Ling; Bi, Chaowei; Cheng, Jiasen
• Is Part Of: Molecular plant pathology. Volume 20:Number 7(2019)
• Page Start: 895
• Page End: 906
• Publication Date: 2019-05-09
• Subjects: oxidative stress -- Sclerotinia sclerotiorum -- Survival factor 1 -- virulence; Plant diseases -- Molecular aspects -- Periodicals; Plant-pathogen relationships -- Molecular aspects -- Periodicals; 571.936
• DOI: 10.1111/mpp.12801
• Languages: English
• ISSNs: 1464-6722

Abstract

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 .