Multiple antibiotic resistance (mar) locus protects Escherichia coli from rapid cell killing by fluoroquinolones.
The multiple antibiotic resistance (mar) locus in Escherichia coli consists of two divergently expressed operons (marC and marRAB), both of which contribute to the Mar phenotype. Overexpression of the marRAB operon protected E. coli against rapid cell killing by fluoroquinolones. Inactivation of the operon in mar mutants restored a wild-type bactericidal susceptibility. Both operons of the locus were required for protection from the quinolone-mediated bactericidal activity in mar locus deletion mutants. The effect was lost at high concentrations of fluoroquinolones, unlike the case for the previously described genes hipA and hipQ. The inducible mar locus appears to specify a novel antibactericidal mechanism which may play a role in the emergence of fluoroquinolone-resistant clinical E. coli isolates.
Goldman
J D
JD
Center for Adaptation Genetics and Drug Resistance, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
White
D G
DG
Levy
S B
SB
D000890:Anti-Infective Agents / Q000494:pharmacology*; D002876:Chromosomes, Bacterial; D004352:Drug Resistance, Microbial / Q000235:genetics*; D018432:Drug Resistance, Multiple / Q000235:genetics*; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics*; D007613:Kanamycin Resistance / Q000235:genetics; D008826:Microbial Sensitivity Tests; D009154:Mutation; D009643:Norfloxacin / Q000494:pharmacology; D009876:Operon; D010641:Phenotype; D010957:Plasmids
D000890:Anti-Infective Agents; D009643:Norfloxacin