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Microbiology 152 (2006), 855-861; DOI  10.1099/mic.0.28385-0
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Microbiology 152 (2006), 855-861; DOI  10.1099/mic.0.28385-0
© 2006 Society for General Microbiology

The impairment of superoxide dismutase coordinates the derepression of the PerR regulon in the response of Staphylococcus aureus to HOCl stress

Sami Maalej1,2, Ines Dammak1 and Sam Dukan2

1 Laboratoire de Microbiologie, Faculté des Sciences de Sfax, 3018 Sfax, Tunisia
2 Laboratoire de chimie bactérienne IBSM, CNRS UPR 9043, 31, chemin Joseph Aiguier, 13402 Marseille Cedex 20, France

Correspondence
Sam Dukan
sdukan{at}ibsm.cnrs-mrs.fr

The response of Staphylococcus aureus to hypochlorous acid (HOCl) exposure was investigated. HOCl challenges were performed on cultures interrupted in the exponential phase. Pretreatment with HOCl conferred resistance to hydrogen peroxide in a PerR-dependent manner. Derepression of the PerR regulon was observed at low HOCl concentration (survival >50 %), using several fusions of different stress promoters to lacZ reporter genes. At least four members of the PerR regulon (katA, mrgA, bcp and trxA) encoding proteins with antioxidant properties were strongly induced following exposure to various HOCl concentrations. A striking result was the link between the derepression of the PerR regulon and the decreased superoxide dismutase (SOD) activity following exposure to increased HOCl concentrations. The sodA mutant was more resistant than the wild-type and also had a higher level of 3-phosphoglycerate dehydrogenase (a measure of PerR regulon activity) without exposure to HOCl. Together, these results imply that derepression of PerR by HOCl is dependent on the level of SOD and protects exponentially arrested cells against HOCl stress.

Abbreviations: 3-PGDH, 3-phosphoglycerate dehydrogenase; SOD, superoxide dismutase




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