The fungal pathogen Ustilago maydis exhibits a dimorphic switch from b
udding to filamentous growth in response to mating interactions and en
vironmental 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 p
resence of cAMP or by extragenic suppression because of a mutation in
the ubc1 gene. The ubc1 gene encodes a type II regulatory subunit of c
AMP-dependent protein kinase (PKA); defects in this gene attenuate the
filamentous growth that normally occurs in response to mating and exp
osure to air. Growth of wild-type cells in cAMP and mutation of the ub
c1 gene also cause defects in the separation of mother and daughter ce
lls (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.