@article{mbs:/content/journal/micro/10.1099/mic.0.26674-0, author = "Lithgow, James K. and Ingham, Eileen and Foster, Simon J.", title = "Role of the hprT–ftsH locus in Staphylococcus aureus", journal= "Microbiology", year = "2004", volume = "150", number = "2", pages = "373-381", doi = "https://doi.org/10.1099/mic.0.26674-0", url = "https://www.microbiologyresearch.org/content/journal/micro/10.1099/mic.0.26674-0", publisher = "Microbiology Society", issn = "1465-2080", type = "Journal Article", abstract = "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.", }