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Eukaryotic Cell, June 2007, p. 931-939, Vol. 6, No. 6
1535-9778/07/$08.00+0 doi:10.1128/EC.00049-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Michael J. Svarovsky,1,
Amy J. Karlsson,1
Joel P. Wagner,1
Karen Marchillo,2
Philip Oshel,3
David Andes,2 and
Sean P. Palecek1*
Department of Chemical & Biological Engineering,1 Department of Medicine,2 Department of Animal Sciences, University of WisconsinMadison, Madison, Wisconsin 537063
Received 19 February 2007/ Accepted 26 March 2007
Candida albicans is the leading cause of systemic fungal infections in immunocompromised humans. The ability to form biofilms on surfaces in the host or on implanted medical devices enhances C. albicans virulence, leading to antimicrobial resistance and providing a reservoir for infection. Biofilm formation is a complex multicellular process consisting of cell adhesion, cell growth, morphogenic switching between yeast form and filamentous states, and quorum sensing. Here we describe the role of the C. albicans EAP1 gene, which encodes a glycosylphosphatidylinositol-anchored, glucan-cross-linked cell wall protein, in adhesion and biofilm formation in vitro and in vivo. Deleting EAP1 reduced cell adhesion to polystyrene and epithelial cells in a gene dosage-dependent manner. Furthermore, EAP1 expression was required for C. albicans biofilm formation in an in vitro parallel plate flow chamber model and in an in vivo rat central venous catheter model. EAP1 expression was upregulated in biofilm-associated cells in vitro and in vivo. Our results illustrate an association between Eap1p-mediated adhesion and biofilm formation in vitro and in vivo.
Published ahead of print on 6 April 2007.
Present address: Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, 200 1st St. SW, Rochester, MN 55905.
Present address: 3M Corporate Research Materials Laboratory, 201-3E-03, St. Paul, MN 55144.
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