My laboratory studies several features of the human opportunistic pathogen Candida albicans and the relationships of these features to its virulence. In particular, we study the transition between the several morphological forms this organism can assume (blastospores, pseudohyphae, and hyphae) and the relationship of these forms to virulence. A second project in the lab involves Candida’s long-standing classification as an “asexual” yeast. We now know that Candida albicans can indeed undergo mating in a mouse host, a feature that, until recently, has simply remained hidden from investigators. We are now studying various aspects of the Candida sexual cycle including the role of the mouse host in this process. We also study a phenomenon called “phenotypic switching” during which Candida strains can change morphologies at relatively high frequencies. Although phenotypic switching is intimately tied to pathogenesis, neither the molecular mechanisms that underlie it, nor the precise roles it plays during infection are known. We also study C. albicans-host interactions using the fruit fly D. melanogaster as a model for the innate immune system. Finally, we study the evolution of virulence by comparing the whole genome transcriptional circuitry of C. albicans with that of its relative, the model, non-pathogenic yeast S. cerevisiae.