Phosphorylative Transduction of Developmental and Pathogenicity-Related Cues in Sclerotinia Sclerotiorum

Sclerotinia sclerotiorum (Lib.) de Bary is among the world's most successful and omnivorous fungal plant pathogens. Included in the more than 400 species of plants reported as hosts to this fungus are canola, alfalfa, soybean, sunflower, dry bean, and potato. The general inability to develop resistant germplasm with these economically important crops to this pathogen has focused attention on the need for a more detailed examination of the pathogenic determinants involved in disease development. This proposal involved experiments that examined the involvement of protein phosphorylation during morphogenesis (hyphal elongation and sclerotia formation) and pathogenesis (oxalic acid). Data obtained from our laboratories during the course of this project substantiates the fact that kinases and phosphatases are involved and important for these processes. A mechanistic understanding of the successful strategy(ies) used by S . sclerotiorum in infecting and proliferating in host plants and this linkage to fungal development will provide targets and/or novel approaches with which to design resistant crop plants including interference with fungal pathogenic development. The original objectives of this grant included: I. Clone the cyclic AMP-dependent protein kinase A (PKA) catalytic subunit gene from S.sclerotiorum and determine its role in fungal pathogenicity, OA production (OA) and/or morphogenesis (sclerotia formation). II. Clone and characterize the catalytic and regulatory subunits of the protein phosphatase PP2A holoenzyme complex and determine their role in fungal pathogenicity and/or morphogenesis as well as linkage with PKA-regulation of OA production and sclerotia formation. III. Clone and characterize the adenylate cyclase-encoding gene from S . sclerotiorum and detennine its relationship to the PKA/PP2A-regulated pathway. IV. Analyze the expression patterns of the above-mentioned genes and their products during pathogenesis and determine their linkage with infection and fungal growth.