Catalase (KatA) and Alkyl Hydroperoxide Reductase (AhpC) Have Compensatory Roles in Peroxide Stress Resistance and Are Required for Survival, Persistence, and Nasal Colonization inStaphylococcus aureus

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Abstract
Oxidative-stress resistance inStaphylococcus aureusis linked to metal ion homeostasis via several interacting regulators. In particular, PerR controls the expression of a regulon of genes, many of which encode antioxidants. Two PerR regulon members,ahpC(alkylhydroperoxide reductase) andkatA(catalase), show compensatory regulation, with independent and linked functions. AnahpCmutation leads to increased H2O2resistance due to greaterkatAexpression via relief of PerR repression. Moreover, AhpC provides residual catalase activity present in akatAmutant. Mutation of bothkatAandahpCleads 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 H2O2in the medium. This leads to DNA damage, the likely cause of the growth defect. Surprisingly, thekatA ahpCmutant is not attenuated in two independent models of infection, which implies reduced oxygen availability during infection. In contrast, both AhpC and KatA are required for environmental persistence (desiccation) and nasal colonization. Thus, oxidative-stress resistance is an important factor in the ability ofS. aureusto persist in the hospital environment and so contribute to the spread of human disease.