Fungal oxalate decarboxylase activity contributes to Sclerotinia sclerotiorum early infection by affecting both compound appressoria development and function. (15th April 2015)

• Record Type: Journal Article
• Authors: Liang, Xiaofei; Moomaw, Ellen W.; Rollins, Jeffrey A.
• Is Part Of: Molecular plant pathology. Volume 16:Number 8(2015:Oct.)
• Page Start: 825
• Page End: 836
• Publication Date: 2015-04-15
• Subjects: Plant diseases -- Molecular aspects -- Periodicals; Plant-pathogen relationships -- Molecular aspects -- Periodicals; 571.936
• DOI: 10.1111/mpp.12239
• Languages: English
• ISSNs: 1464-6722

Abstract

<abstract abstract-type="main"> <title>Summary</title> <p> <italic>Sclerotinia sclerotiorum</italic> pathogenesis requires the accumulation of high levels of oxalic acid (OA). To better understand the factors affecting OA accumulation, two putative oxalate decarboxylase (OxDC) genes (<italic>Ss‐odc1</italic> and <italic>Ss‐odc2</italic>) were characterized. <italic>Ss‐odc1</italic> transcripts exhibited significant accumulation in vegetative hyphae, apothecia, early stages of compound appressorium development and during plant colonization. <italic>Ss‐odc2</italic> transcripts, in contrast, accumulated significantly only during mid to late stages of compound appressorium development. Neither gene was induced by low pH or exogenous OA in vegetative hyphae. A loss‐of‐function mutant for <italic>Ss‐odc1</italic> (Δ<italic>ss‐odc1</italic>) showed wild‐type growth, morphogenesis and virulence, and was not characterized further. Δ<italic>ss‐odc2</italic> mutants hyperaccumulated OA <italic>in vitro</italic>, were less efficient at compound appressorium differentiation and exhibited a virulence defect which could be fully bypassed by wounding the host plant prior to inoculation. All Δ<italic>ss‐odc2</italic> phenotypes were restored to the wild‐type by ectopic complementation. An <italic>S. sclerotiorum</italic> strain overexpressing <italic>Ss‐odc2</italic> exhibited strong OxDC, but no oxalate oxidase activity. Increasing inoculum nutrient levels increased compound appressorium development, but not penetration efficiency, of Δ<italic>ss‐odc2</italic> mutants. Together, these results demonstrate differing roles for <italic>S. sclerotiorum</italic> OxDCs, with Odc2 playing a significant role in host infection related to compound appressorium formation and function.</p> </abstract>