期刊
MOLECULAR MICROBIOLOGY
卷 71, 期 1, 页码 198-211出版社
WILEY
DOI: 10.1111/j.1365-2958.2008.06518.x
关键词
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资金
- Mochida Memorial Foundation for Medical Pharmaceutical Research
- NIAID
- NIH [R01 AI074658]
- Medical Scientist National Research Service at the University of Chicago [T32GM07281]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI074658] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007281] Funding Source: NIH RePORTER
Oxidative stress serves as an important host/environmental signal that triggers a wide range of responses from the human pathogen Staphylococcus aureus. Among these, a thiol-based oxidation sensing pathway through a global regulator MgrA controls the virulence and antibiotic resistance of the bacterium. Herein, we report a new thiol-based oxidation sensing and regulation system that is mediated through a parallel global regulator SarZ. SarZ is a functional homologue of MgrA and is shown to affect the expression of similar to 87 genes in S. aureus. It uses a key Cys residue, Cys-13, to sense oxidative stress and to co-ordinate the expression of genes involved in metabolic switching, antibiotic resistance, peroxide stress defence, virulence, and cell wall properties. The discovery of this SarZ-mediated regulation, mostly independent from the MgrA-based regulation, fills a missing gap of oxidation sensing and response in S. aureus.
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