Fink Laboratory

Fungi are increasingly the cause of death as there are few effective fungal antibiotics. Fungi gain entry to the body by adhering to indwelling devices such as catheters. The adhesion is intimately linked to the É¿-glucan and the mannoproteins (adhesins) molecules that encase the fungal cell. The analysis of adhesion and filamentation in the model system, Saccharomyces cerevisiae guides our studies in the less tractable pathogen, Candida albicans. The genomes of both fungi encode many mannoproteins that confer unique adherence properties. These adhesins are required for interactions of fungal cells with each other (flocculation and filamentation), with inert surfaces (agar and plastic) and with mammalian cells. These cell surface molecules are the antigens recognized by the phagocytic cells of the immune system. Fungi are able to vary these cell surface molecules. Recent work has shown that antisense RNA plays a key role in the expression of these cell surface molecules. We use genetics, biochemistry and genomics to address questions such as: What mechanisms generate the diversity of cell surface molecules? What cell surface molecules are recognized by the cells of the immune system? How do macrophages and neutrophils distinguish between a pathogen, Candida albicans, and a non-pathogen, Saccharomyces cerevisia.