Published April 12, 2002 | Published
Journal Article Open

Characterization and expression analysis of Staphylococcus aureus pathogenicity island 3 - Implications for the evolution of staphylococcal pathogenicity islands

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Abstract

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."

Additional Information

© 2002 by The American Society for Biochemistry and Molecular Biology, Inc. Received for publication, December 6, 2001, and in revised form, January 3, 2002. Published, JBC Papers in Press, January 30, 2002. We thank Barbara May for assistance with reverse transcription-PCR and Peter Southern for helpful discussions regarding SaPI evolutionary models. Preliminary sequence data were obtained from The Institute for Genomic Research website (www.tigr.org) with support provided by the National Institute of Allergy and Infectious Diseases and Merck Genome Research Institute. 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. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EBI Data Bank with accession number(s) AF410775. [J.M.Y. was] [s]upported by a Howard Hughes Predoctoral Fellowship in the Biological Sciences.

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