Abstract
Ozone is one of the major city air pollutants. Since it is known to induce the overexpression of superoxide-dismutase in various models, and is also a powerful oxidant, we tested if ozone can induce the expression of the soxRS regulon of Escherichia coli, which is activated by superoxide and nitric oxide. A sub-lethal exposure to ozone was unable to activate the expression of soxS'::lacZ transcriptional fusions. However, cells lacking the soxRS locus were more susceptible than wild-type to ozone-mediated killing. Constitutive expression of the soxRS regulon did not increase the resistance to ozone. Ozone might be exerting a selective pressure upon oxidative-stress defense mechanisms in airborne bacteria.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Bacterial Proteins / genetics*
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Bacterial Proteins / metabolism
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Enzyme Induction
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Escherichia coli / drug effects
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Escherichia coli / genetics*
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Escherichia coli / metabolism
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Escherichia coli Proteins*
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Gene Expression Regulation, Bacterial
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Isopropyl Thiogalactoside / pharmacology
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Ozone / pharmacology*
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Plasmids
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Recombinant Fusion Proteins / metabolism
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Regulon*
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Superoxide Dismutase / biosynthesis
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Trans-Activators*
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Transcription Factors / genetics*
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Transcription Factors / metabolism
Substances
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Bacterial Proteins
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Escherichia coli Proteins
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Recombinant Fusion Proteins
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Trans-Activators
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Transcription Factors
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SoxR protein, Bacteria
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SoxS protein, E coli
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Isopropyl Thiogalactoside
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Ozone
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Superoxide Dismutase