Signaling and morphogenesis of pathogenic fungi
Our lab is investigating the molecular mechanisms that promote the pathogenesis of the human fungal pathogen Candida albicans. Lethal systemic infections caused by C. albicans are on the rise as new medical treatments are increasing the pool of susceptible individuals. The pathogenic effects of C. albicans are caused by its ability to grow in the host and disseminate to internal organs. An underlying factor is the ability of C. albicans to respond to signals from the host to induce virulence functions. This includes a switch in morphology from round budding cells to elongated hyphae that facilitates invasive growth into tissues. The pathways that stimulate hyphal growth also induce the expression of virulence factors that promote attachment to host cells and resist the attack of the host immune system. Therefore, our studies focus on defining the mechanisms that regulate cell signaling and morphogenesis.
One current area of research is to define the mechanisms by which C. albicans responds to the sugar GlcNAc to induce hyphal formation and virulence gene expression. These studies also have significance for understanding the emerging roles of GlcNAc signaling in human disease and in the regulation of pathogenic fungi and bacteria.
We are also studying the role of the plasma membrane, as this essential barrier mediates secretion of virulence factors, morphogenesis, cell wall synthesis, and interfaces with the extracellular environment. These studies are expected to aid in development of novel therapeutic approaches by providing new insight into the mechanisms underlying C. albicans pathogenesis and also by providing a better understanding of the mechanisms of current antifungal drugs that target the plasma membrane.