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J. Biol. Chem., Vol. 277, Issue 15, 13138-13147, April 12, 2002
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From the We describe the complete sequence of the
15.9-kb staphylococcal pathogenicity island 3 encoding
staphylococcal enterotoxin serotypes B, K, and Q. The island, which
meets the generally accepted definition of pathogenicity islands,
contains 24 open reading frames potentially encoding proteins of more
than 50 amino acids, including an apparently functional integrase. The
element is bordered by two 17-bp direct repeats identical to those
found flanking staphylococcal pathogenicity island 1. The island has
extensive regions of homology to previously described pathogenicity
islands, particularly staphylococcal pathogenicity islands 1 and bov.
The expression of 22 of the 24 open reading frames contained on
staphylococcal pathogenicity island 3 was detected either in
vitro during growth in a laboratory medium or serum or in
vivo in a rabbit model of toxic shock syndrome using DNA
microarrays. The effect of oxygen tension on staphylococcal
pathogenicity island 3 gene expression was also examined. By
comparison with the known staphylococcal pathogenicity islands in the
context of gene expression described here, we propose a model of
pathogenicity island origin and evolution involving specialized
transduction events and addition, deletion, or recombination of
pathogenicity island "modules."
The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EBI Data Bank with accession number(s) AF410775.
Characterization and Expression Analysis of
Staphylococcus aureus Pathogenicity Island 3
IMPLICATIONS FOR THE EVOLUTION OF STAPHYLOCOCCAL PATHOGENICITY
ISLANDS*
§,

,
,
**
Department of Microbiology, University of
Minnesota Medical School, Minneapolis, Minnesota 55455, and
¶ Department of Veterinary Pathobiology and Biomedical Genomics
Center, University of Minnesota, St. Paul, Minnesota 55108
*
This work was supported in part by National Institutes of
Health Grant AI22159 (to P. M. S.).The costs of publication of this article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Present address: Dept. of Environmental Science and
Engineering, California Institute of Technology, 209 Keck Laboratories, M/C 138-78, Pasadena, CA 91125-7800.
**
To whom correspondence should be addressed: Dept. of Microbiology,
University of Minnesota Medical School, MMC 196, 420 Delaware St. SE,
Minneapolis, MN 55455. Tel.: 612-624-9471; Fax: 612-626-0623; E-mail:
pats@lenti.med.umn.edu.

Present address: The Lawson Health Research Inst., The
University of Western Ontario, Grosvenor Campus, 268 Grovenor Street, Rm. H-323, London, Ontario, Canada N6A4V2.
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