Candida albicans is an opportunistic fungal pathogen and the major cause of human fungal infections. It resides commensally on the mucosal tissues of the human body in immunocompetent individuals. However, it is also responsible for causing superficial mucosal infections and life-threatening systemic infections, particularly in those who are immunocompromised. The morphology of this fungus changes from a yeast form to pseudohyphae and true hyphae. The transition from the yeast form to the filamentous forms is linked to virulence. C. albicans responds to environmental signals to alter its cell morphology, switching from the yeast form to the filamentous forms (termed the dimorphic transition). A number of factors have been identified that serve as triggers for this transition including pH, temperature, starvation for nitrogen, amino acid levels, and the presence of serum. Understanding how the cell senses and responds to its environment is important in understanding its pathogenesis. We are investigating a transcription factor that, when mutated, blocks the ability of the cell to undergo the dimorphic transition. This mutant also exhibits decreased virulence. We plan to investigate changes in gene expression through northern analysis and micro-array studies. We will identify the target genes through chromatin immunoprecipitation. We will also determine the epistatic relationship between this gene and other genes known to be involved in hyphal formation.
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