Genetic analysis of biofilm formation in Saccharomyces
cerevisiae .
Todd Reynolds, Kexin Yu, Gerald Fink
Whitehead Institute, M.I.T., 9 Cambridge Center, Cambridge, MA 02142,
United States of America
The fungal pathogen Candida albicans has become a major cause of
hospital-acquired (nosocomial) infections. Intravascular catheters are
strongly associated with Candida infections because
Candida forms biofilms on these devices. Biofilms form when
microbes that were free in liquid (planktonic) adhere to a suitable
substrate (initiation), and grow as a surface-attached community. The
biofilm form of Candida is more resistant to antifungal agents
resulting in persistent infections. We are using Saccharomyces
cerevisiae to model the initation phase of fungal biofilm formation
with 96-well plates as a substrate. We have found that Flo11p, a member
of a large family of fungal cell-surface glycoprotiens that includes
several Candida virulence factors, is necessary for adhesion of
Saccharomyces to polystyrene. Flo11p is involved in filamentous
growth in yeast and pathways known to regulate FLO11 during
filamentous growth also influence biofilm initiation. Analogous pathways
in C. albicans effect biofilm formation by Candida in a
similar manner. Microarray analysis of S. cerevisiae comparing
adherent and non-adherent cells revealed that several genes known to
regulate FLO11 including RAS2 and TEC1 were
upregulated in the adherent population. In addition, a rho-type GTPase,
RHO5, was revealed that perturbs adhesion to polystyrene when
disrupted. We are characterizing the role of RHO5 and other
genes revealed by microarray analysis in biofilm formation.
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