Candida glabrata is a species of opportunistic pathogenic yeast which is often found on the epithelium and typically causes infections in immunocompromised individuals, which are often treated with antifungal drugs such as azoles. C. glabrata is increasing in medical relevance as it is the second most common pathogen responsible for candida infections. Like many pathogens, C. glabrata has developed resistance to the drugs used to treat patients, namely fluconazole. Azole drugs target the ergosterol biosynthesis pathway, specifically an enzyme encoded by the gene ERG11. Studies have shown that regulation of the membrane transporter Cdr1 is the basis of azole resistance and that hyperactive mutant forms of the transcription factor Pdr1 can upregulate CDR1 expression. Our lab aims to understand how Pdr1 is regulated in order to understand how azole resistance develops and functions in the pathogen. We are investigating this regulation in two ways. First, the lab has identified a number of proteins which co-purify with Pdr1, one of which is Spt5, which we are studying to determine how they regulate Pdr1 activity, leading to azole resistance. We are investigating this regulation by developing auxin-inducible conditional depletion mutants of the co-activator proteins to quantify PDR1 expression when the co-activators are depleted under azole stress condidtions. We expect that depletion of such proteins will decrease PDR1 expression and activity. The lab is also performing high-throughput screening of a compound library to find compounds which perturb CDR1 expression in wild-type and gain of function Pdr1 strains. In order to detect these expression changes, we are using strains which contain a CDR1 promoter-controlled luciferase reporter. In this screen, we expect to find compounds which significantly decrease CDR1 expression and impact regulation in the Pdr1-Cdr1 network leading to an altered azole resistance phenotype. This research will further our understanding of the mechanisms of azole resistance and may lead to improvements in treating azole resistant pathogens.