Fungal oxalate decarboxylase activity contributes to Sclerotinia sclerotiorum early infection by affecting both compound appressoria development and function.

ABSTRACT: Sclerotinia sclerotiorum 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 (Ss-odc1 and Ss-odc2) were characterized. Ss-odc1 transcripts exhibited significant accumulation in vegetative hyphae, apothecia, early stages of compound appressorium development and during plant colonization. Ss-odc2 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 Ss-odc1 (?ss-odc1) showed wild-type growth, morphogenesis and virulence, and was not characterized further. ?ss-odc2 mutants hyperaccumulated OA?in?vitro, 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 ?ss-odc2 phenotypes were restored to the wild-type by ectopic complementation. An S.?sclerotiorum strain overexpressing Ss-odc2 exhibited strong OxDC, but no oxalate oxidase activity. Increasing inoculum nutrient levels increased compound appressorium development, but not penetration efficiency, of ?ss-odc2 mutants. Together, these results demonstrate differing roles for S.?sclerotiorum?OxDCs, with Odc2 playing a significant role in host infection related to compound appressorium formation and function.

SUBMITTER: Liang X 

PROVIDER: S-EPMC6638544 | biostudies-literature | 2015 Oct

REPOSITORIES: biostudies-literature