ABSTRACT

Ustilago maydis, the causal agent of corn smut disease, displays dimorphic growth in which it alternates between a budding haploid saprophyte and a filamentous dikaryotic pathogen. Our laboratory has been focused on utilizing this dimorphic growth transition as a morphological marker for understanding the disease process. In this minireview we describe work primarily from our laboratory carried out over the last several years that, in the context of the greater research effort on this and other fungal-plant pathosystems, has begun to produce a framework regarding signal transduction as a critical factor in fungal disease development. We have identified a role for the cAMP signal transduction pathway in the dimorphic switch. Haploids mutant in the uac 1 gene encoding adenylate cyclase are converted from budding to constitutively filamentous. Mutagenesis of the uac 1 disruption strain allowed the isolation of a large number of budding suppressor mutants named ubc, for Ustilago bypass of cyclase because they no longer require cAMP for budding growth. Analysis of these suppressor mutants led to the identification of 5 genes that are required for filamentous growth. One of these (ubc 1) encodes the regulatory subunit of the cAMP dependent protein kinase. Three genes, ubc3, ubc4 and ubc 5 encode members of a MAP kinase cascade with highest similarity to those of the yeast pheromone response pathway. Finally, the ubc2 gene, when mutated, produces a similar phenotype to the ubc3 through ubc5 utants and it interacts genetically with ubc4. We therefore propose that the ubc2 gene is a novel protein involved in pheromone response. We describe the roles of uac 1 and the ubc genes in morphogenesis, mating and in pathogenicity. Additionally, we have isolated a number of fungal transcripts that are expressed at specific morphological stages. We are also in the process of isolating host and pathogen genes induced in the formation of plant galls.