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Infect Immun, June 1998, p. 2871-2878, Vol. 66, No. 6
Laboratory of Bacterial Pathogenesis and
Immunology, The Rockefeller University, New York, New York 10021
Received 15 December 1997/Returned for modification 13 March
1998/Accepted 20 March 1998
Coagulase-negative staphylococci are common nosocomial pathogens. A
regulatory element, designated sar, partially controls exoprotein synthesis in coagulase-positive Staphylococcus
aureus by modulating the expression of another regulatory locus,
called agr. We report here the cloning of a sar
homolog in S. epidermidis. The major open reading frame
within sar in S. epidermidis is highly homologous (84%) to the S. aureus SarA protein. Primer
extension studies revealed three sar transcripts (0.64, 0.76, and 0.85 kb) initiated from three distinct promoters. The
interpromoter region in S. epidermidis differs from its
S. aureus counterpart, possibly suggesting target gene
differences and a disparate pattern for sar activation.
Remarkably, the S. epidermidis sar homolog interacts with
an agr promoter fragment of S. aureus in gel
shift assays. Additionally, S. epidermidis sar fragments
could restore hemolysin production in an S. aureus sar
mutant. As typical virulence determinants controlled by sar
in S. aureus are not present in S. epidermidis, an examination of functional and structural similarities and divergence of sar in staphylococci will be of major interest.
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Characterization of a sar Homolog of
Staphylococcus epidermidis

and
*
Corresponding author. Mailing address: The Laboratory
of Bacterial Pathogenesis and Immunology, The Rockefeller University, 1230 York Ave., New York, NY 10021. Phone: (212) 327-8163. Fax: (212)
327-7385. E-mail: cheunga{at}rockvax.rockefeller.edu.
Present address: Department of Internal Medicine, Abteilung
für Infektiologie, Kantonsspital Basel, CH-4031 Basel,
Switzerland.
Present address: Hygiene Institut, 72074 Tübingen,
Germany.
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