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• W2101366952 endingPage "e1000760" @default.
• W2101366952 startingPage "e1000760" @default.
• W2101366952 abstract "Bacteria can survive antibiotic treatment without acquiring heritable antibiotic resistance. We investigated persistence to the fluoroquinolone ciprofloxacin in Escherichia coli. Our data show that a majority of persisters to ciprofloxacin were formed upon exposure to the antibiotic, in a manner dependent on the SOS gene network. These findings reveal an active and inducible mechanism of persister formation mediated by the SOS response, challenging the prevailing view that persisters are pre-existing and formed purely by stochastic means. SOS-induced persistence is a novel mechanism by which cells can counteract DNA damage and promote survival to fluoroquinolones. This unique survival mechanism may be an important factor influencing the outcome of antibiotic therapy in vivo." @default.
• W2101366952 created "2016-06-24" @default.
• W2101366952 creator A5014027005 @default.
• W2101366952 creator A5052038207 @default.
• W2101366952 creator A5089532497 @default.
• W2101366952 date "2009-12-11" @default.
• W2101366952 modified "2023-10-12" @default.
• W2101366952 title "SOS Response Induces Persistence to Fluoroquinolones in Escherichia coli" @default.
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• W2101366952 doi "https://doi.org/10.1371/journal.pgen.1000760" @default.
• W2101366952 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2780357" @default.
• W2101366952 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20011100" @default.
• W2101366952 hasPublicationYear "2009" @default.
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