Genome-Wide Transcriptional Response of Staphylococcus Aureus to Hypochlorite-Induced Oxidative Stress
Wook Chang1, Freshteh Toghrol2, and William E. Bentley1. (1) Center for Biosystems Research, University of Maryland Biotechnology Institute, 701 Mapes Rd, Ft. Meade, MD 20755, (2) Office of Pesticide Programs, U.S. Environmental Protection Agency, 701 Mapes Rd, Ft. Meade, MD 20755
Staphylococcus aureus, a pathogen capable of causing life-threatening endocarditis and toxic shock syndrome, encounters toxicity from phagocyte-derived reactive oxidative species such as hypochlorite and hydrogen peroxide during active infection. S. aureus responds with adaptive and protective strategies against these toxic species to effectively infect humans. Despite advances in our understanding of the responses to oxidative stress in many specific cases, the connectivity between targeted protective genes and the rest of cell metabolism remains obscure. Therefore, herein, we reported the transcriptome analysis of the cellular response of S. aureus to hypochlorite–driven oxidative stress by using Affymetrix GeneChip arrays. In particular, we demonstrated how global gene expression profiles changed during the time course after the stress. Our data showed that (1) genes involved in cell wall synthesis, membrane transport, and primary metabolism were continuously downregulated; (2) amino acid synthesis genes were initially upregulated; (3) virulence factor genes were selectively induced throughout the growth inhibition; and (4) aminoacyl-tRNA biosynthesis genes were initially downregulated, whereas genes associated with ribosomal protein synthesis were specifically repressed afterward. Moreover, we revealed gene expression signatures between hypochlorite- and hydrogen peroxide-inducible oxidative responses in S. aureus. Finally, the results presented herein may facilitate the further elucidation of the mechanisms involved in S. aureus-host interactions.