CAMP REGULATES MORPHOGENESIS IN THE FUNGAL PATHOGEN USTILAGO-MAYDIS

The fungal pathogen Ustilago maydis exhibits a dimorphic switch from budding to filamentous growth in response to mating interactions and environmental conditions. We have found that disruption of the uac1 gene, encoding adenylate cyclase, results in a constitutively filamentous phenotype. Budding is restored to the uac1 mutant upon growth in the presence of cAMP or by extragenic suppression because of a mutation in the ubc1 gene. The ubc1 gene encodes a type II regulatory subunit of cAMP-dependent protein kinase (PKA); defects in this gene attenuate the filamentous growth that normally occurs in response to mating and exposure to air. Growth of wild-type cells in cAMP and mutation of the ubc1 gene also cause defects in the separation of mother and daughter cells (cytokinesis) and alter bud site selection. These results indicate a key role for cAMP and PKA in morphogenesis in U. maydis; this role may be common among dimorphic fungal pathogens.