ibclogo XVI International Botanical Congess


Abstract Number: 4199
Session = 12.15.6


THE ROLE OF CAMP SIGNALING IN THE MORPHOGENESIS AND PATHOGENESIS OF USTILAGO MAYDIS


Mario Moniz de Sa, Adriana De Maria, Nancy Lee, Dave Laidlaw, Yume Khono, James Kronstad. Biotechnology Laboratory, University of British Columbia, 237-6174 University Blvd, Vancouver, BC, Canada V6T 123


Ustilago maydis is a dimorphic basidiomycete and the causative agent of corn smut disease. It alternates between a diploid filamentous, pathogenic stage and a haploid, nonpathogenic budding growth stage. The cAMP signal transduction pathway is essential in the life cycle of this fungus, playing a key role in this dimorphic switch, as well as in pathogenicity, bud-site selection and mating. Many genes encoding key components of this pathway have been cloned and characterized. Adenylyl cyclase (uac1) mutants display constitutively filamentous growth. Budding growth can be rescued by exogenous cAMP. Suppressor analysis of uac1 mutants identified the regulatory subunit of PKA (ubc1). ubc1 mutants show a multiple budding phenotype and, although infectious, are defective for tumor formation. The gene encoding the main catalytic subunit of PKA (adr1) has also been identified. Mutants defective in adr1 display a filamentous phenotype and are nonpathogenic. We are focusing on identifying downstream targets of PKA using suppressor analysis and subtraction cDNA libraries. Some of these genes include hgl1, which has several PKA phosphorylation sites and has been identified as a putative target of PKA. hgl1 mutants display a budding phenotype and although pathogenic, fail to form teliospores. Another gene, lip1, encodes a lipase and appears to be negatively regulated by hgl1.


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