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The enterococcus faecalis fsr two-component system controls biofilm development through production of gelatinase

Academic Article
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Overview

authors

  • Hancock, L. E.
  • Perego, Marta

publication date

  • September 2004

journal

  • Journal of Bacteriology  Journal

abstract

  • Bacterial growth as a biofilm on solid surfaces is strongly associated with the development of human infections. Biofilms on native heart valves (infective endocarditis) is a life-threatening disease as a consequence of bacterial resistance to antimicrobials in such a state. Enterococci have emerged as a cause of endocarditis and nosocomial infections despite being normal commensals of the gastrointestinal and female genital tracts. We examined the role of two-component signal transduction systems in biofilm formation by the Enterococcus faecalis V583 clinical isolate and identified the fsr regulatory locus as the sole two-component system affecting this unique mode of bacterial growth. Insertion mutations in the fsr operon affected biofilm formation on two distinct abiotic surfaces. Inactivation of the fsr-controlled gene gelE encoding the zinc-metalloprotease gelatinase was found to prevent biofilm formation, suggesting that this enzyme may present a unique target for therapeutic intervention in enterococcal endocarditis.

subject areas

  • Adaptation, Physiological
  • Bacterial Proteins
  • Biofilms
  • Enterococcus faecalis
  • Gelatinases
  • Gene Expression Regulation, Bacterial
  • Gene Order
  • Genes, Bacterial
  • Genes, Regulator
  • Mutagenesis, Insertional
  • Mutation
  • Operon
  • Protein Kinases
  • Serine Endopeptidases
  • Signal Transduction
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Identity

International Standard Serial Number (ISSN)

  • 0021-9193

Digital Object Identifier (DOI)

  • 10.1128/jb.186.17.5629-5639.2004

PubMed ID

  • 15317767
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Additional Document Info

start page

  • 5629

end page

  • 5639

volume

  • 186

issue

  • 17

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