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Manganese-dependent regulation of the endocarditis-associated virulence factor EfaA of Enterococcus faecalis

¹Department of Pharmacy and Pharmacology, University of Bath, Bath BA2 7AY, UK ²Department of Oral and Dental Science, University of Bristol, Bristol BS1 2LY, UK

Correspondence Anthony W. Smith a.w.smith{at}bath.ac.uk

Received 31 July 2002 Accepted 22 October 2002

There is increasing recognition of the emerging role of manganese regulation and acquisition in some pathogenic bacteria. Expression of the Enterococcus faecalis endocarditis-associated virulence factor EfaA is induced by growth in serum. It is demonstrated here that expression of the efaCBA operon encoding a putative ABC-type transporter is regulated by Mn²⁺. Transcription of efaCBA and EfaA production were repressed in Mn²⁺-supplemented medium. A Mn²⁺-responsive transcriptional regulator, EfaR, sharing 27 % identity with the Corynebacterium diphtheriae diphtheria toxin repressor (DtxR), was identified. In the presence of Mn²⁺, EfaR protein bound in vitro to the efaC promoter region. Analysis of the E. faecalis V583 genome revealed ten additional putative EfaR-binding sites, suggesting that manganese availability could have a broader regulatory role in infection. The results identify a new Mn²⁺-sensing regulator in enterococci that regulates the expression of a virulence factor implicated in enterococcal endocarditis.

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