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Microbiology 150 (2004), 373-381; DOI  10.1099/mic.0.26674-0
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Microbiology 150 (2004), 373-381; DOI  10.1099/mic.0.26674-0
© 2004 Society for General Microbiology

Role of the hprT–ftsH locus in Staphylococcus aureus

James K. Lithgow1, Eileen Ingham2 and Simon J. Foster1

1 Department of Molecular Biology and Biotechnology, University of Sheffield, Sheffield S10 2TN, UK
2 Department of Microbiology, University of Leeds, Leeds LS2 9JT, UK

Correspondence
Simon J. Foster
s.foster{at}sheffield.ac.uk

The roles of two adjacent genes in the Staphylococcus aureus chromosome with functions in starvation survival and the response to stressful conditions have been characterized. One of these, hprT, encoding a hypoxanthine–guanine phosphoribosyltransferase homologue, was initially identified in a transposon mutagenesis screen. Mutation of hprT affects starvation survival in amino-acid-limiting conditions and the ability of S. aureus to grow in high-salt concentrations. Downstream of hprT is ftsH, which encodes a membrane-bound, ATP- and Zn2+-dependent ‘AAA’-type protease. Mutation of ftsH in S. aureus leads to pleiotropic defects including slower growth, sensitivity to salt, acid, methyl viologen and potassium tellurite stresses, and reduced survival in amino-acid- or phosphate-limiting conditions. Both hprT–lacZ and ftsH–lacZ gene fusions are expressed maximally in the post-exponential phase of growth. Although secretion of exoproteins is not affected, an ftsH mutant is attenuated in a murine skin lesion model of pathogenicity.




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