The CuZn superoxide dismutase from Sclerotinia sclerotiorum is involved with oxidative stress tolerance, virulence, and oxalate production

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• 作者：Selvakumar Veluchamy^a ; ¹ ; Brett Williams^a ; ^b ; ¹ ; Kyoungsu Kim^a ; ^c ; Martin B. Dickman^a ; ^{mbdickman@tamu.edu}
• 关键词：Superoxide dismutase ; Oxalate ; Sclerotinia sclerotioum ; Oxidative stress tolerance ; Reactive oxygen species
• 刊名：Physiological and Molecular Plant Pathology
• 出版年：2012
• 期刊代码：183_08855765
• 类别：bio
• 出版时间：April, 2012
• 卷：78
• 期：Complete
• 页码：14-23
• 文件大小：1472 K

摘要

One of the earliest plant responses to pathogens is the induced accumulation of reactive oxygen species (ROS). The superoxide ion is an important intermediate in the generation of ROS having a key regulatory function during plant-microbe interactions and is an important component in fungal development. The superoxide dismutase (SOD) family contributes to frontline defense via detoxification of reactive superoxide radical anions. Sclerotinia sclerotiorum (Lib.) de Bary is a necrotrophic fungal pathogen with a broad host range. S.聽sclerotiorum produces the non-specific phytotoxin and key pathogenicity factor, oxalic acid (OA). We have identified an S.聽sclerotiorum SOD (Sssod1) with high similarity to CuZnSODs. Sssod1 contains an open reading frame of 908聽bp in length and is predicted to encode a protein of 155 amino acids that harbors the entire hallmark motifs associated with SOD function. Treatment with the CuZnSOD inhibitor diethyldithiocarbamate (DETC) resulted in delayed hyphal growth and sclerotial development in a dose-dependent manner. Mutants generated carrying an Sssod1 deletion (螖Sssod1) exhibited morphological defects similar to those observed with the inhibitor treatment. Moreover, 螖Sssod1 was more sensitive than wild-type to menadione, a redox cycling agent. Expression of Sssod1 was induced following treatment with oxidizing agents and during interaction with plant host tissue the 螖Sssod1 mutant was significantly reduced in virulence on both tomato and tobacco plants compared to wild-type. Interestingly, pathogenicity of the superoxide dismutase mutant was mostly restored following supplementation with oxalate. We also observed that 螖Sssod1 was reduced in oxalate production by half. In accordance with reduced virulence, 螖Sssod1 induced a host oxidative burst in adjacent uninfected cells, a phenotype indicative of active pathogen recognition by the host. Intriguingly, during wild-type infection, host ROS production was significantly reduced. These results suggest that wild-type Sclerotinia suppresses host defense responses during infection.