Abstract
Enterococcus faecalis is a natural inhabitant of the human gastrointestinal tract. However, as an opportunistic pathogen, it is able to colonize other host niches and cause life-threatening infections. Its adaptation to new environments involves global changes in gene expression. The EF3013 gene (here named mafR) of E. faecalis strain V583 encodes a protein (MafR, 482 residues) that has sequence similarity to global response regulators of the Mga/AtxA family. The enterococcal OG1RF genome also encodes the MafR protein (gene OG1RF_12293). In this work, we have identified the promoter of the mafR gene using several in vivo approaches. Moreover, we show that MafR influences positively the transcription of many genes on a genome-wide scale. The most significant target genes encode components of PTS-type membrane transporters, components of ABC-type membrane transporters, and proteins involved in the metabolism of carbon sources. Some of these genes were previously reported to be up-regulated during the growth of E. faecalis in blood and/or in human urine. Furthermore, we show that a mafR deletion mutant strain induces a significant lower degree of inflammation in the peritoneal cavity of mice, suggesting that enterococcal cells deficient in MafR are less virulent. Our work indicates that MafR is a global transcriptional regulator. It might facilitate the adaptation of E. faecalis to particular host niches and, therefore, contribute to its potential virulence.
Highlights
The Gram-positive bacterium Enterococcus faecalis is usually found among the commensal microflora of the human gastrointestinal tract
Our understanding of the mechanisms involved in the pathogenicity of E. faecalis is still very limited
We show that MafR has a positive effect on the utilization of glycerol, maltose, and mannitol, suggesting that MafR may facilitate the survival of E. faecalis in particular host niches
Summary
The Gram-positive bacterium Enterococcus faecalis is usually found among the commensal microflora of the human gastrointestinal tract. It can become pathogenic and cause a variety of community-acquired and health care-associated infections, such as urinary tract infections, endocarditis, and bacteraemia. Compared to V583, the OG1RF genome contains 227 unique open reading frames but has fewer mobile genetic elements. Both enterococcal strains have contributed to the identification of numerous factors important for virulence (Fisher and Phillips, 2009). Global transcriptional regulators that respond to specific external signals are crucial in the adaptation of pathogenic bacteria to different host niches
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