title: SOS response induces persistence to fluoroquinolones in Escherichia coli.
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.
authors.affiliation: Antimicrobial Discovery Center, Department of Biology, Northeastern University, Boston, Massachusetts, USA.
authors.forename: Tobias
authors.initials: T
authors.lastname: Dörr
authors.forename: Kim
authors.initials: K
authors.lastname: Lewis
authors.forename: Marin
authors.initials: M
authors.lastname: Vulić
mesh_terms: D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D002939:Ciprofloxacin / Q000494:pharmacology*; D004352:Drug Resistance, Microbial / Q000235:genetics; D004926:Escherichia coli / Q000187:drug effects* / Q000235:genetics; D013014:SOS Response, Genetics; D013269:Stochastic Processes
chemical_list: D000900:Anti-Bacterial Agents; D002939:Ciprofloxacin