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Journal of Bacteriology, August 2009, p. 5147-5158, Vol. 191, No. 16
0021-9193/09/$08.00+0     doi:10.1128/JB.00401-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Overexpression of VpsS, a Hybrid Sensor Kinase, Enhances Biofilm Formation in Vibrio cholerae{triangledown} ,{dagger}

Nicholas J. Shikuma,1,{ddagger} Jiunn C. N. Fong,1,{ddagger} Lindsay S. Odell,1,{ddagger} Barrett S. Perchuk,2 Michael T. Laub,2 and Fitnat H. Yildiz1*

Department of Microbiology and Environmental Toxicology, University of California, Santa Cruz, Santa Cruz, California 05964,1 Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 021392

Received 24 March 2009/ Accepted 2 June 2009

Vibrio cholerae causes the disease cholera and inhabits aquatic environments. One key factor in the environmental survival of V. cholerae is its ability to form matrix-enclosed, surface-associated microbial communities known as biofilms. Mature biofilms rely on Vibrio polysaccharide to connect cells to each other and to a surface. We previously described a core regulatory network, which consists of two positive transcriptional regulators, VpsR and VpsT, and a negative transcriptional regulator HapR, that controls biofilm formation by regulating the expression of vps genes. In this study, we report the identification of a sensor histidine kinase, VpsS, which can control biofilm formation and activates the expression of vps genes. VpsS required the response regulator VpsR to activate vps expression. VpsS is a hybrid sensor histidine kinase that is predicted to contain both histidine kinase and response regulator domains, but it lacks a histidine phosphotransferase (HPT) domain. We determined that VpsS acts through the HPT protein LuxU, which is involved in a quorum-sensing signal transduction network in V. cholerae. In vitro analysis of phosphotransfer relationships revealed that LuxU can specifically reverse phosphotransfer to CqsS, LuxQ, and VpsS. Furthermore, mutational and phenotypic analyses revealed that VpsS requires the response regulator LuxO to activate vps expression, and LuxO positively regulates the transcription of vpsR and vpsT. The induction of vps expression via VpsS was also shown to occur independent of HapR. Thus, VpsS utilizes components of the quorum-sensing pathway to modulate biofilm formation in V. cholerae.

* Corresponding author. Mailing address: Department of Microbiology and Environmental Toxicology, University of California, Santa Cruz, Santa Cruz, CA 95064. Phone: (831) 459-1588. Fax: (831) 459-3524. E-mail: yildiz{at}metx.ucsc.edu

{triangledown} Published ahead of print on 12 June 2009.

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.

{ddagger} N.J.S., J.C.N.F., and L.S.O. contributed equally to this work.

Journal of Bacteriology, August 2009, p. 5147-5158, Vol. 191, No. 16
0021-9193/09/$08.00+0     doi:10.1128/JB.00401-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Yang, M., Frey, E. M., Liu, Z., Bishar, R., Zhu, J. (2010). The Virulence Transcriptional Activator AphA Enhances Biofilm Formation by Vibrio cholerae by Activating Expression of the Biofilm Regulator VpsT. Infect. Immun. 78: 697-703 [Abstract] [Full Text]  


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