EfaR is a major regulator of Enterococcus faecalis manganese transporters and influences processes involved in host colonization and infection.

Metal ions, in particular manganese, are important modulators of bacterial pathogenicity. However, little is known about the role of manganese-dependent proteins in the nosocomial pathogen Enterococcus faecalis, a major cause of bacterial endocarditis. The present study demonstrates that the DtxR/MntR family metalloregulator EfaR of E. faecalis controls the expression of several of its regulon members in a manganese-dependent way. We also show that efaR inactivation impairs the ability of E. faecalis to form biofilms, to survive inside macrophages, and to tolerate oxidative stress. Our results reveal that EfaR is an important modulator of E. faecalis virulence and link manganese homeostasis to enterococcal pathogenicity.
AuthorsM C Abrantes, J Kok, M de F Lopes
JournalInfection and immunity (Infect Immun) Vol. 81 Issue 3 Pg. 935-44 (Mar 2013) ISSN: 1098-5522 [Electronic] United States
PMID23297382 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Bacterial Proteins
  • Cation Transport Proteins
  • Metals
  • Manganese
  • Animals
  • Bacterial Proteins (genetics, metabolism)
  • Biological Transport (physiology)
  • Cation Transport Proteins (genetics, metabolism)
  • Cell Line, Tumor
  • Enterococcus faecalis (genetics, metabolism, pathogenicity)
  • Gene Expression Regulation, Bacterial (drug effects, physiology)
  • Macrophages
  • Manganese (metabolism)
  • Metals (pharmacology)
  • Multigene Family
  • Oligonucleotide Array Sequence Analysis
  • Virulence

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