Volume 275, Issue 2 pp. 199-206

vpsA- and luxO-independent biofilms of Vibrio cholerae

Jana Müller

Jana Müller

Department of Civil & Environmental Engineering, Stanford University, Stanford, CA, USA

Search for more papers by this author
Michael C. Miller

Michael C. Miller

Department of Microbiology and Immunology, Stanford University, Stanford, CA, USA

Search for more papers by this author
Alex T. Nielsen

Alex T. Nielsen

Department of Microbiology and Immunology, Stanford University, Stanford, CA, USA

Search for more papers by this author
Gary K. Schoolnik

Gary K. Schoolnik

Department of Microbiology and Immunology, Stanford University, Stanford, CA, USA

Search for more papers by this author
Alfred M. Spormann

Alfred M. Spormann

Department of Civil & Environmental Engineering, Stanford University, Stanford, CA, USA

Departments of Biological Sciences, Chemical Engineering and Geological and Environmental Sciences, Stanford University, Stanford, CA, USA

Search for more papers by this author
First published: 22 August 2007
Citations: 7
Correspondence: Alfred M. Spormann, James H. Clark Center for Biomedical Engineering and Science, Stanford University, Stanford, CA 9405-5429, USA. Tel.: +1 650 723 3668; fax: +1 650 724 4927; e-mail: [email protected]

Editor: Mark Schembri

Abstract

The natural life cycle of Vibrio cholerae involves the transitioning of cells between different environmental surfaces such as the chitinous shell of Crustaceae and the epithelial layer of the human intestine. Previous studies using static biofilm systems showed a strict dependence of biofilm formation on the vps and lux genes, which are essential for exopolysaccharide formation and cell–cell signaling, respectively. The authors' report here that in biofilms grown under hydrodynamic conditions, ΔvpsA and ΔluxO mutants of V. cholerae do form pronounced, three-dimensional biofilms that resemble all aspects of wild-type biofilms. By genetic experiments, it was shown that in hydrodynamically grown biofilms this independence of vpsA is due to the expression of rpoS, which is a negative regulator of vpsA expression. Biofilms also underwent substantial dissolution after 96 h that could be induced by a simple stop of medium flow. The studies indicate that metabolic conditions control the reversible attachment of cells to the biofilm matrix and are key in regulating biofilm cell physiology via RpoS. Furthermore, the results redefine the roles of vps and quorum-sensing in V. cholerae biofilms.

The full text of this article hosted at iucr.org is unavailable due to technical difficulties.