Abstract Detail

Molecular mechanisms of adaptation to host and environment

Liang, Xiaofei [1], Liberti, Daniele [2], Li, Moyi [3], Kim, Young-Tae [4], Hutchens, Andrew [5], Wilson, Ron [1], Rollins, Jeffrey [1].

Genetic Regulation of Oxalate Metabolism in Sclerotinia sclerotiorum.

The successful infection of the devastating and broad host range necrotrophic fungal plant pathogen Sclerotinia sclerotiorum involves production and secretion of oxalic acid (OA). We have characterized, a peroxisomal carnitine acetyl transferase gene (Ss-pth2) required for metabolizing fatty acid or 2-C carbon substrates for OA production. Its function suggests the glyoxylate cycle contributes to OA biogenesis under restricted nutrient conditions. To further dissect the genetic regulation of OA metabolism and pathogenesis of S. sclerotiorum, the putative oxaloacetate acetylhydrolase gene Ss-oah1 and the putative oxalate decarboxylase genes, Ss-odc1 and Ss-odc2, were functionally characterized. Neutral pH strongly induces Ss-oah1 transcript accumulation and this pH induction is completely suppressed in the ambient pH signaling mutant ΔSs-pac1. ΔSs-oah1 mutants fail to accumulate OA and show dramatically reduced virulence upon plant inoculation. These phenotypes are rescued by complementation with the wild type Ss-oah1 gene. The Ss-odc1 and Ss-odc2 genes showed no inductive transcripts accumulation in response to either low pH (3.0) or exogenous OA (up to 40 mM at pH 4.8). Ss-odc2 transcripts, but not Ss-odc1transcripts, showed strong and specific induction during compound appressorium differentiation. No growth, morphogenesis, or virulence phenotypic changes were observed for the ΔSs-odc1 mutant while ΔSs-odc2 mutants exhibited less efficient compound appressorium differentiation, increased OA accumulation, and significantly reduced virulence. The virulence defect of the ΔSs-odc2 mutants could be fully restored by wounding prior to inoculation. Taken together, our observations indicate the S. sclerotiorum infection involves a fine-tuned regulation of OA accumulation by genetic factors regulating both OA biogenesis and OA catabolism.

1 - University of Florida, Plant Pathology, Fifield hall, PO Box 110680, Hull Road, Gainesville, Florida, 32611-0680, United States
2 - Bayer CropScience Nunhems Netherlands, PO Box 4005, Haelen, 6080, Netherlands
3 - University of Florida, Department of Molecular Genetics and Microbiology, Gainesville, Florida
4 - Environmental Biotechnology Research Centre, 125 Gwahak-Ro, Yuseong-Gu, Daejeon, 305-806, Republic of Korea
5 - University of Maryland, Medical center, 22 S. Greene Street, Baltimore, MD, USA

Keywords:
Oxalic acid
Sclerotinia sclerotiorum
Pathogenicity
Metabolism.

Presentation Type: Symposium or Colloquium Presentation
Session: SY5
Location: Room 103 AB/Kellogg Hotel and Conference Center
Date: Tuesday, June 10th, 2014
Time: 2:00 PM
Number: SY5003
Abstract ID:61
Candidate for Awards:None