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Transcriptional Regulator PerA Influences Biofilm-Associated, Platelet Binding, and Metabolic Gene Expression in Enterococcus faecalis

Authors
Journal
PLoS ONE
1932-6203
Publisher
Public Library of Science
Publication Date
Volume
7
Issue
4
Identifiers
DOI: 10.1371/journal.pone.0034398
Keywords
  • Research Article
  • Biology
  • Genetics
  • Gene Expression
  • Dna Transcription
  • Microbiology
  • Bacteriology
  • Bacterial Biofilms
  • Bacterial Pathogens
  • Host-Pathogen Interaction
  • Immunity
  • Microbial Metabolism
  • Microbial Pathogens
  • Microbial Physiology
  • Molecular Cell Biology
  • Medicine
  • Infectious Diseases
  • Bacterial Diseases
  • Enterococcus Infection

Abstract

Enterococcus faecalis is an opportunistic pathogen and a leading cause of nosocomial infections, traits facilitated by the ability to quickly acquire and transfer virulence determinants. A 150 kb pathogenicity island (PAI) comprised of genes contributing to virulence is found in many enterococcal isolates and is known to undergo horizontal transfer. We have shown that the PAI-encoded transcriptional regulator PerA contributes to pathogenicity in the mouse peritonitis infection model. In this study, we used whole-genome microarrays to determine the PerA regulon. The PerA regulon is extensive, as transcriptional analysis showed 151 differentially regulated genes. Our findings reveal that PerA coordinately regulates genes important for metabolism, amino acid degradation, and pathogenicity. Further transcriptional analysis revealed that PerA is influenced by bicarbonate. Additionally, PerA influences the ability of E. faecalis to bind to human platelets. Our results suggest that PerA is a global transcriptional regulator that coordinately regulates genes responsible for enterococcal pathogenicity.

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