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J. Bacteriol. doi:10.1128/JB.01832-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

YcfR (BhsA) Influences Escherichia coli Biofilm Formation Through Stress Response and Surface Hydrophobicity

Artie McFerrin Department of Chemical Engineering, the Department of Biology, and the Zachry Department of Civil Engineering

^* To whom correspondence should be addressed. Email: Thomas.Wood{at}chemail.tamu.edu.

	Abstract

DNA microarrays revealed that expression of ycfR, which encodes a putative outer membrane protein, is significantly induced in E. coli biofilms and is also induced by several stress conditions. We show that deletion of ycfR increased biofilm formation 5-fold in the presence of glucose; the glucose effect was corroborated by showing binding of the cAMP receptor protein to the ycfR promoter. It appears that YcfR is a multiple stress resistance protein since deleting ycfR also renders the cell more sensitive to acid, heat treatment, hydrogen peroxide, and cadmium. Stress increasing biofilm formation through YcfR appears to be the result of decreasing indole synthesis since a mutation in the tnaA gene encoding tryptophanase prevents enhanced biofilm formation upon stress, and adding indole prevents enhanced biofilm upon stress. Deleting ycfR also affected outer membrane proteins and converted the cell from hydrophilic to hydrophobic, as well as increased cell aggregation 4-fold. YcfR seems to be involved in the regulation of E. coli K-12 biofilm formation by decreasing cell aggregation and cell-surface adhesion, by influencing the concentration of signal molecules, and by interfering with stress responses. Based on our findings, we propose this locus to be named bhsA for influencing biofilm through hydrophobicity and stress response.

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