This Article Full Text Full Text (PDF) Other Versions of this Article: JB.00859-07v1 189/20/7262    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Shanks, R. M. Q. Articles by Nau, G. J. Search for Related Content PubMed PubMed Citation Articles by Shanks, R. M. Q. Articles by Nau, G. J.

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, Pennsylvania 15213,¹ Department of Molecular Genetics and Biochemistry, University of Pittsburgh, Pittsburgh, Pennsylvania 15261,² Department of Pharmacology and Genetics, Dartmouth Medical School, Lebanon, New Hampshire 03756,³ Center for Biological Imaging, Department of Cell Biology and Physiology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261⁴

Received 2 June 2007/ Accepted 26 July 2007

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 fimbria structural genes were identified. S. marcescens oxyR mutants were severely impaired in biofilm formation, in contrast to the hyperbiofilm 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 fimbrial genes resulted in severe defects in fimbria-associated phenotypes, revealing roles in cell-cell and cell-biotic surface interactions. Transmission electron microscopy revealed the absence of fimbria-like surface structures on an OxyR-deficient strain and an enhanced fimbrial phenotype in strains bearing oxyR on a multicopy plasmid. The hyperfimbriated phenotype conferred by the multicopy oxyR plasmid was absent in a type I fimbrial mutant background. Real-time reverse transcriptase PCR indicated an absence of transcripts from a fimbrial operon in an oxyR mutant that were present in the wild type and a complemented oxyR mutant strain. Lastly, chromosomal P_lac-mediated expression of fimABCD 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 fimbrial gene expression.

Published ahead of print on 3 August 2007.

This article has been cited by other articles:

• Kalivoda, E. J., Stella, N. A., O'Dee, D. M., Nau, G. J., Shanks, R. M. Q. (2008). The Cyclic AMP-Dependent Catabolite Repression System of Serratia marcescens Mediates Biofilm Formation through Regulation of Type 1 Fimbriae. Appl. Environ. Microbiol. 74: 3461-3470 [Abstract] [Full Text]