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^B Regulates IS256-Mediated Staphylococcus aureus Biofilm Phenotypic Variation

Jaione Valle,^1, Marta Vergara-Irigaray,¹ Nekane Merino,¹ José R. Penadés,² and Iñigo Lasa^1*

Laboratory of Microbial Biofilms, Instituto de Agrobiotecnología, and Departamento de Producción Agraria, Universidad Pública de Navarra-CSIC, Pamplona-31006, Spain,¹ Instituto Valenciano de Investigaciones Agrarias (IVIA) and Cardenal Herrera-CEU University, 46113 Moncada, Valencia, Spain²

Received 20 November 2006/ Accepted 23 January 2007

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 for generating 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 ^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 chromosomes of biofilm-negative variants, as well as with an augmented IS256 insertion frequency into the icaC and the sarA genes. IS256-mediated biofilm switching is reversible, and biofilm-positive variants could emerge from biofilm-negative ^B mutants. Analysis of the chromosomal insertion frequency using a recombinant IS256 element tagged with an erythromycin marker showed an 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.

Published ahead of print on 2 February 2007.

Present address: Groupe de Génétique des Biofilms. Institut Pasteur, URA CNRS 2172, Paris 75724, France.

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