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James Konopka

James Konopka Professor

Ph.D., University of California/ Los Angeles, 1985
370 Life Sciences Building

 

E-mail:
Office:
Fax:

james.konopka@stonybrook.edu
(631) 632-8715
(631) 632-9797

 

Publications

Research

Molecular mechanisms of fungal pathogenesis

Our lab investigates 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 biofilm formation and invasive growth into tissues.  The pathways that stimulate hyphal growth also induce the expression of virulence factors that promote attachment to host cells and resistance to attack by the host immune system.  Our studies focus on defining the mechanisms that regulate cell signaling and morphogenesis to promote fungal virulence. 

One current area of research is to define the broad roles of the plasma membrane in C. albicans pathogenesis.  This essential barrier mediates secretion of virulence factors, morphogenesis, cell wall synthesis, and interfaces with the extracellular environment.  We are also studying a new antioxidant pathway that protects the plasma membrane from attack by the host immune system.  These studies are identifying new avenues for development of antifungal drugs and are providing a better understanding of the mechanisms of current antifungal drugs that will enable them to be used more effectively.

Another goal of our work is to define the mechanisms by which C. albicans responds to the sugar N-acetylglucosamine (GlcNAc).  This amino sugar is a potent inducer of hyphal formation and virulence gene expression in C. albicans.  These studies also have significance for understanding the emerging roles of GlcNAc signaling the regulation of other pathogenic microbes and in human disease.