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Elevated levels of ^S inhibit biofilm formation in Escherichia coli: a role for the Rcs phosphorelay

Lionel Ferrières^1,

¹ Molecular Microbiology Laboratory, Department of Biology and Biochemistry, University of Bath, Bath BA2 7AY, UK
² Department of Microbiology and Alimentary Pharmabiotic Centre, University College Cork, Ireland

The Rcs phosphorelay is composed of RcsC, RcsD and the response regulator RcsB, and this signalling pathway has been implicated in virulence and biofilm formation in many enteric bacteria. It was previously shown that a mutation in rcsC resulted in defective biofilm formation in Escherichia coli [Ferrières, L. & Clarke, D. J. (2003) Mol Microbiol 50, 1665–1682]. To identify the molecular mechanisms underlying the observed biofilm defect we carried out a screen looking for suppressor mutants that restored biofilm formation in the rcsC mutant background. One of the mutants was identified to be in rprA, a gene encoding a small RNA molecule that is involved in the post-transcriptional control of the alternative sigma factor, ^S. The expression of rprA is regulated by the Rcs phosphorelay, and there are elevated ^S levels present in the rcsC mutant due to the overexpression of rprA in this background. Using different approaches, we have established that the increase in ^S levels is responsible for the biofilm defect. Therefore, the Rcs phosphorelay is involved in maintaining appropriate levels of ^S during biofilm formation in E. coli.

Correspondence
David J. Clarke
Email: david.clarke{at}ucc.ie

Present address: Unité de Génétique des Biofilms, Département de Microbiologie, URA CNRS 2172, Institut Pasteur, 25 rue du Dr Roux, 75724 Paris cedex 15, France.

Figures demonstrating that mutations in rcsC and rcsD reduce expression of flhDC and motility, colanic acid production is not responsible for the biofilm defect observed in the rcsC mutant background, the deletion of rprA restores ^s levels in the rcsC mutant, and the RprA-mediated increase in the level of ^S is not responsible for the decrease in motility, are available with the online version of this paper.