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J. Bacteriol. doi:10.1128/JB.01524-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Catalase (KatA) and alkyl hydroperoxide reductase (AhpC) have compensatory roles in peroxide stress resistance and are required for survival, persistence and nasal colonisation in Staphylococcus aureus

Department of Molecular Biology and Biotechnology, University of Sheffield, Western Bank, Sheffield, S10 2TN, UK; Department of Rheumatology and Inflammation research, Göteborg University, Göteborg, Sweden; Biosynexus Incorporated, 9119 Gaither Road, Gaithersburg, Maryland 20877, USA

^* To whom correspondence should be addressed. Email: S.Foster{at}sheffield.ac.uk.

	Abstract

Oxidative stress resistance in Staphylococcus aureus is linked to metal ion homeostasis via several interacting regulators. In particular PerR controls expression of a regulon of genes, many of which encode antioxidants. Two PerR regulon members ahpC (alkylhydroperoxide reductase) and katA (catalase), show compensatory regulation, with independent and linked functions. An ahpC mutation leads to increased H₂O₂ resistance due to greater katA expression via relief of PerR repression. Moreover, AhpC provides residual catalase activity present in a katA mutant. Mutation of both katA and ahpC leads to a severe growth defect under aerobic conditions in defined media (attributable to lack of catalase activity). This results in the inability to scavenge exogenous or endogenously produced H₂O₂, resulting in accumulation of H₂O₂ in the medium. This leads to DNA damage, the likely cause of the growth defect. Surprisingly the katA ahpC mutant is not attenuated in two independent models of infection, which alludes to reduced oxygen availability during infection. In contrast both AhpC and KatA are required for environmental persistence (desiccation) and nasal colonisation. Thus, oxidative stress resistance is an important factor in the ability of S. aureus to persist in the hospital environment and so contribute to the spread of human disease.

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