4.8 Article

Regulation of cell-surface genes and biofilm formation by the C-albicans transcription factor Bcr1p

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CURRENT BIOLOGY
卷 15, 期 12, 页码 1150-1155

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CELL PRESS
DOI: 10.1016/j.cub.2005.05.047

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  1. NIAID NIH HHS [R01AI050931, R21AI055823] Funding Source: Medline

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The impact of many microorganisms on their environment depends upon their ability to form surface bound communities called biofilms [1]. Biofilm formation on implanted medical devices has severe consequences for human health by providing both a portal of entry and a sanctuary for invasive bacterial and fungal pathogens [1, 2]. Biofilm regulators and adherence molecules are extensively defined for many bacterial pathogens [3-5], but not for fungal pathogens such as Candida albicans. Elongated filaments called hyphae are a prominent feature of C. albicans biofilms, and known genes that promote biofilm formation are required for hyphal development [2, 6-8]. From a new library of transcription-factor mutants' we identify Bcr1p, a zinc finger protein required for formation of biofilms but not hyphae. Expression analysis shows that Bcr1p activates cell-surface protein and adhesin genes, including several induced during hyphal development. BCR1 expression depends upon the hyphal regulator Tec1p. Thus, BCR1 is a downstream component of the hyphal regulatory network that couples expression of cell-surface genes to hyphal differentiation. Our results indicate that hyphal cells are specialized to present adherence molecules that support biofilm integrity.

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