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The response regulator PhoP negatively regulates Yersinia pseudotuberculosis and Yersinia pestis biofilms

Yi-Cheng Sun1, Alexandra Koumoutsi, Creg Darby

  • 1Department of Cell and Tissue Biology, Program in Microbial Pathogenesis, University of California, San Francisco, CA, USA.

FEMS Microbiology Letters
|November 26, 2008
PubMed

Insights

A mutation in the phoP gene enables Yersinia pseudotuberculosis to form biofilms on Caenorhabditis elegans. Deleting phoP in wild-type strains also induced biofilm formation, highlighting PhoP

Area of Science:

  • Microbiology
  • Bacteriology
  • Molecular Biology

Background:

  • Yersinia pseudotuberculosis exhibits variable biofilm formation on Caenorhabditis elegans.
  • The genetic basis for biofilm formation in Y. pseudotuberculosis is not fully understood.

Purpose of the Study:

  • To investigate the role of the phoP gene in Yersinia pseudotuberculosis biofilm formation on C. elegans.
  • To determine the impact of phoP mutations on biofilm development in Yersinia species.

Main Methods:

  • Genetic manipulation of Yersinia strains (Y. pseudotuberculosis and Yersinia pestis) including gene deletion.
  • Biofilm assays using the nematode Caenorhabditis elegans as a model.
  • Analysis of HmsT diguanylate cyclase expression.

Main Results:

  • A mutation in the phoP gene was identified as the cause of biofilm-positive phenotype in Y. pseudotuberculosis strain YPIII.
  • Deletion of the phoP gene in wild-type Y. pseudotuberculosis strains induced robust biofilm formation on C. elegans.
  • PhoP mutants of Yersinia pestis showed increased in vitro biofilm formation compared to wild-type.
  • Functional PhoP in Y. pseudotuberculosis diminished the expression of HmsT, a key biofilm regulator.

Conclusions:

  • The response regulator PhoP plays a significant inhibitory role in Yersinia biofilm formation on C. elegans.
  • PhoP acts by downregulating the expression of HmsT, a diguanylate cyclase essential for biofilm development.
  • Targeting the PhoP-HmsT pathway could be a strategy to control Yersinia biofilm formation.

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