Candida auris is an emerging fungal pathogen responsible for healthcare-associated outbreaks driven by persistent colonization, and characterized by high levels of resistance to antifungal treatment. We study the molecular and cellular basis of C. auris persistence, transmission, and disease. By working with diverse clinical isolates from global outbreaks, we investigate within-species variation and the evolutionary pressures that have made this organism such a formidable nosocomial threat. Our goal is to understand what makes this organism a successful pathogen so that we can design ways to prevent disease.

Functional genomic screens use mutant collections and phenotypic screening to find genes that control interesting behavior. In  fungal pathogens, interesting behavior can include regulation of virulence factors, such as filamentation, or growth in a stressful condition, such as the host. We are also interested in factors that contribute to spread and transmission of fungal pathogens. We are building genome-scale mutant libraries in C. auris to enable unbiased, organism-wide screens for these clinically relevant traits. These approaches let us move beyond potentially biasde candidate gene studies to discover unexpected contributors to pathogenesis.

Although C. albicans, C. auris, and C. neoformans are exciting human fungal pathogens, a current downside is that many open reading frames (ORFs) are still uncharacterized, and many do not have clear homologues in other organisms, making them both mysterious and potentially pathogen-specific. We integrate large-scale datasets (transcriptomics, proteomics, imaging, whole-genome sequencing) with molecular genetics and cell biology to assign functions to these understudied genes. Deciphering the “dark genome” of fungal pathogens opens the door to novel biology and new antifungal targets.