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Microbiology and Molecular Biology Reviews, June 2009, p. 233-248, Vol. 73, No. 2
1092-2172/09/$08.00+0     doi:10.1128/MMBR.00005-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

At the Crossroads of Bacterial Metabolism and Virulence Factor Synthesis in Staphylococci

Greg A. Somerville^1* and Richard A. Proctor^2,

Department of Veterinary and Biomedical Sciences, University of Nebraska—Lincoln, Lincoln, Nebraska,¹ University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin²

Summary: Bacteria live in environments that are subject to rapid changes in the availability of the nutrients that are necessary to provide energy and biosynthetic intermediates for the synthesis of macromolecules. Consequently, bacterial survival depends on the ability of bacteria to regulate the expression of genes coding for enzymes required for growth in the altered environment. In pathogenic bacteria, adaptation to an altered environment often includes activating the transcription of virulence genes; hence, many virulence genes are regulated by environmental and nutritional signals. Consistent with this observation, the regulation of most, if not all, virulence determinants in staphylococci is mediated by environmental and nutritional signals. Some of these external signals can be directly transduced into a regulatory response by two-component regulators such as SrrAB; however, other external signals require transduction into intracellular signals. Many of the external environmental and nutritional signals that regulate virulence determinant expression can also alter bacterial metabolic status (e.g., iron limitation). Altering the metabolic status results in the transduction of external signals into intracellular metabolic signals that can be "sensed" by regulatory proteins (e.g., CodY, Rex, and GlnR). This review uses information derived primarily using Bacillus subtilis and Escherichia coli to articulate how gram-positive pathogens, with emphasis on Staphylococcus aureus and Staphylococcus epidermidis, regulate virulence determinant expression in response to a changing environment.

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* Corresponding author. Mailing address: Dept. of Veterinary and Biomedical Sciences, University of Nebraska—Lincoln, 155 VBS, Fair St. and East Campus Loop, Lincoln, NE 68583-0905. Phone: (402) 472-6063. Fax: (402) 472-9690. E-mail: gsomerville3{at}unl.edu

Present address: Merck Research Laboratories, North Wales, PA.

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Microbiology and Molecular Biology Reviews, June 2009, p. 233-248, Vol. 73, No. 2
1092-2172/09/$08.00+0     doi:10.1128/MMBR.00005-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

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