Research in the Cowen lab exploits model and pathogenic fungi to address mechanisms by which global cellular regulators alter the relationship between genotype and phenotype in an environmentally contingent manner, influencing evolution, drug resistance, development, and infectious disease.

Much of our work focuses on Hsp90, an essential molecular chaperone that regulates the form and function of diverse client proteins, many of which are key regulators of cellular signaling. We found that Hsp90 potentiates the evolution and maintenance of drug resistance by enabling specific cellular signaling pathways and crucial responses to the cellular stress exerted by antifungal drugs. We are now dissecting the key signaling cascades downstream of Hsp90 as well as epigenetic mechanisms by which Hsp90 function is regulated. We discovered that Hsp90 regulates temperature-dependent developmental transitions from yeast to filamentous growth in pathogenic fungi. Our studies suggest that impairing fungal stress response pathways holds great promise for treating life-threatening fungal infectious diseases.