CDK regulation of transcriptional repression by Efg1 in Candida
Allen Yi-Jen Wang, University of California, Irvine
Candida albicans is the most commonly isolated human fungal pathogen and is responsible for both disseminated and superficial infections. Immuno-compromised individuals, including patients undergoing chemotherapy and those suffering from AIDS, are particularly susceptible to Candida infections. In fact, over 90% of AIDS patients suffer from oral candidiasis over the course of the disease. Due to the increasing resistance of C. albicans to the commonly used anti-fungal drugs fluconazole and amphotericin-B, the necessity to better understand the virulence properties of C. albicans is of much greater importance. One virulence property of C. albicans has been attributed to its unique ability to undergo a morphogenic switch from a yeast growth form to a hyphal growth form. A key regulator of this switch is the transcription factor Efg1. Efg1 is essential for the morphogenic switch as the deletion of this gene from C. albicans results in a strain that cannot under go the yeast to hyphal transition in most growth conditions. It has been observed that Efg1 has both transcriptional activation and repression activities. How these activities of Efg1 are regulated is not known. Our preliminary data suggest that the ability of Efg1 to act as a repressor is regulated by CDK. The objective of this research is to determine the molecular mechanisms of the Efg1-mediated transcriptional repression and to ascertain the effect this activity has on morphogenesis.