This Article Full Text (PDF) Other Versions of this Article: JB.01767-06v1 189/7/2886    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 Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Valle, J. Articles by Lasa, I. Search for Related Content PubMed PubMed Citation Articles by Valle, J. Articles by Lasa, I.

 Previous Article  |  Next Article 

J. Bacteriol. doi:10.1128/JB.01767-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

^B regulates IS256-mediated Staphylococcus aureus biofilm phenotypic variation

Laboratory of Microbial Biofilms. Instituto de Agrobiotecnología and Dpto. de Producción Agraria, Universidad Pública de Navarra-CSIC. Pamplona-31006, Spain; Instituto Valenciano de Investigaciones Agrarias (IVIA) and Cardenal Herrera-CEU University, 46113 Moncada, Valencia, Spain

^* To whom correspondence should be addressed. Email: ilasa{at}unavarra.es.

	Abstract

Biofilm formation in Staphylococcus aureus is subject to phase variation and biofilm-negative derivatives emerge sporadically from a biofilm-positive bacterial population. To date, the only known mechanism to generate biofilm phenotypic variation in staphylococci is the reversible insertion/excision of IS256 in biofilm-essential genes. In this study, we present evidence suggesting that the absence of the s^B transcription factor dramatically increases the rate of switching to the biofilm-negative phenotype in the clinical isolate S. aureus 15981, under both steady-state and flow conditions. The phenotypic switching correlates with a dramatic increase in the number of IS256 copies in the chromosome of biofilm-negative variants, as well as with an augmented IS256 insertion frequency into the icaC and the sarA genes. The IS256-mediated biofilm switching is reversible and biofilm positive variants could emerge from biofilm negative s^B mutants. Analysis of the chromosomal insertion frequency using recombinant IS256r tagged with an erythromycin marker showed almost three times higher transposition frequency in a ^B strain. However, regulation of IS256 activity by ^B appears to be indirect, since transposase transcription is not affected in the absence of ^B and IS256 activity is inhibited to wild type levels in a ^B strain under NaCl stress. Overall, our results identify a new role for ^B as a negative regulator of insertion sequence transposition and support the idea that deregulation of IS256 activity abrogates biofilm formation capacity in S. aureus.

This article has been cited by other articles:

• Nagorska, K., Hinc, K., Strauch, M. A., Obuchowski, M. (2008). Influence of the {sigma}B Stress Factor and yxaB, the Gene for a Putative Exopolysaccharide Synthase under {sigma}B Control, on Biofilm Formation. J. Bacteriol. 190: 3546-3556 [Abstract] [Full Text]  
• Plague, G. R., Dunbar, H. E., Tran, P. L., Moran, N. A. (2008). Extensive Proliferation of Transposable Elements in Heritable Bacterial Symbionts. J. Bacteriol. 190: 777-779 [Abstract] [Full Text]  
• Palmer, R. J. Jr., Stoodley, P. (2007). Biofilms 2007: Broadened Horizons and New Emphases. J. Bacteriol. 189: 7948-7960 [Full Text]  
• Tormo, M. A., Ubeda, C., Marti, M., Maiques, E., Cucarella, C., Valle, J., Foster, T. J., Lasa, I., Penades, J. R. (2007). Phase-variable expression of the biofilm-associated protein (Bap) in Staphylococcus aureus. Microbiology 153: 1702-1710 [Abstract] [Full Text]