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J. Bacteriol. doi:10.1128/JB.00859-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

A Serratia marcescens OxyR homolog mediates surface attachment and biofilm formation

Charles T. Campbell Laboratory of Ophthalmic Microbiology, Department of Ophthalmology, UPMC Eye Center, Pittsburgh, PA 15213, Department of Molecular Genetics and Biochemistry, University of Pittsburgh, Pittsburgh, PA 15261, Department of Pharmacology and Genetics, Dartmouth Medical School, Lebanon, NH, 03756, Center for Biological Imaging, Department of Cell Biology and Physiology, University of Pittsburgh, Pittsburgh, PA 15261

^* To whom correspondence should be addressed. Email: shanksrm{at}upmc.edu.

	Abstract

OxyR is a conserved bacterial transcription factor with a regulatory role in oxidative stress response. From a genetic screen for genes that modulate biofilm formation in the opportunistic pathogen Serratia marcescens, mutations in an oxyR homolog and predicted fimbriae structural genes were identified. S. marcescens oxyR mutants were severely impaired in biofilm formation, as opposed to the hyper-biofilm phenotype exhibited by oxyR mutants of Escherichia coli and Burkholderia pseudomallei. Further analysis revealed that OxyR plays a role in the primary attachment of cells to a surface. Similar to what is observed in other bacterial species, S. marcescens OxyR is required for oxidative stress resistance. Mutations in oxyR and type I fimbriae genes conferred severe defects in fimbriae-associated phenotypes revealing roles in cell-cell and cell-biotic surface interactions. Transmission electron microscopy revealed the absence of fimbriae-like surface structures on an OxyR-deficient strain and an enhanced fimbriae phenotype in strains bearing oxyR on a multicopy plasmid. The hyper-fimbriated phenotype conferred by the multicopy oxyR plasmid was absent in a type I fimbriae mutant background. Real time RT-PCR indicates an absence of transcript from a fimbriae operon in an oxyR mutant that are present in the wild type and a complemented oxyR mutant strain. Lastly, chromosomal P_lac-mediated expression of fimbriae was sufficient to restore wild-type levels of yeast agglutination and biofilm formation to an oxyR mutant. Together these data support a model in which OxyR contributes to early stages of S. marcescens biofilm formation by influencing fimbriae gene expression.

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