Cryptococcus neoformans is a major opportunistic fungal pathogen in AIDS and other immunosuppressed patients. We have shown that wild-type haploid C. neoformans can develop an extensive hyphal phase under appropriate conditions. Hyphae produced under these conditions are monokaryotic, possess unfused clamp connections, and develop basidia with viable basidiospores. The ability to undergo this transition is determined by the presence of the a-mating type locus and is independent of serotype. The association of the hyphal phase with the a-mating type may explain the preponderance of this mating type in the environment and the nature of the infectious propagule of C. neoformans.Since the discovery of the sexual or perfect state of the human fungal pathogen Cryptococcus neoformans by Kwon-Chung (1, 2), it has been considered a bipolar heterothallic basidiomycete with two mating types, a and a (MA Ta and MA Ta The ability of hyphae to form fruiting body-like structures in the vegetative phase is called monokaryotic, homokaryotic, or haploid fruiting (13). Although haploid fruiting is common in the higher basidiomycetes (13-15), it has not been characterized in C. neoformans, and association with mating type has never been described. Recent observations made in this laboratory and a reassessment of past studies (5, 10, 16) allow us to propose a new hypothesis for the biased mating type ratios and the nature of the infectious propagule of C. neoformans. We show here that a strains of C. neoformans can undergo a true dimorphic transition from a haploid yeast phase to a hyphal phase from which vegetative growth can continue indefinitely. The hyphal phase is induced by nitrogen starvation on a solid surface. Basidia bearing viable basidiospores are also produced, all of which are a in mating type. The ability of a but not a cells to form basidiospores under these conditions provides an attractive explanation for both the mating type bias and the nature of the infectious propagule of C. neoformans. MATERIALS AND METHODSStrains. The strains used in this study are listed in Table 1. Auxotrophic strains were derived from JEC20 (MA Ta) and JEC21 (MA Ta). JEC20 and JEC21 are a well-characterized, haploid, congenic pair of prototrophic laboratory strains that presumably differ only at the mating type locus (17).Media 7327The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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SummaryUstilago maydis, the causal agent of corn smut disease, displays dimorphic growth in which it alternates between a budding haploid saprophyte and a ®la-mentous dikaryotic pathogen. We are interested in identifying the genetic determinants of ®lamentous growth and pathogenicity in U. maydis. To do this, we have taken a forward genetic approach. Previously, we showed that haploid adenylate cyclase (uac1) mutants display a constitutively ®lamentous phenotype. Mutagenesis of a uac1 disruption strain allowed the isolation of a large number of budding suppressor mutants. These mutants are named ubc, for Ustilago bypass of cyclase, as they no longer require the production of cAMP to grow in the budding morphology. Complementation of one of these suppressor mutants led to the identi®cation of ubc3, which is required for ®lamentous growth and encodes a MAP kinase most similar to those of the yeast pheromone response pathway. In addition to ®lamentous growth, the ubc3 gene is required for pheromone response and for full virulence. Mutations in the earlier identi®ed fuz7 MAP kinase kinase also suppress the ®lamentous phenotype of the uac1 disruption mutant, adding evidence that both ubc3 and fuz7 are members of this same MAP kinase cascade. These results support an important interplay of the cAMP and MAP kinase signal transduction pathways in the control of morphogenesis and pathogenicity in U. maydis.

The Aspergillus nidulans wA gene is required for synthesis of a green pigment present in the walls of mature asexual spores (conidia); wA mutants produce colorless (white) conidia. We determined the transcriptional structure and DNA sequence of the wA gene. wA consists of 5 exons separated by short (40-60 bp) introns. The processed transcript has the potential to encode a protein consisting of 1986 amino acid residues. The predicted WA polypeptide showed extensive sequence similarities with bacterial and fungal polyketide synthases and vertebrate fatty acid synthases, particularly within conserved active sites. Properties of the yellow conidial wall pigment intermediate suggest that it is a polyketide rather than a fatty acid. It is therefore likely that wA encodes all or part of a polyketide synthase involved in the formation of this pigment intermediate.

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