Novel mechanism for fluoroquinolone resistance in Acinetobacter baumannii.
An EZ::TN<R6Kγori/KAN-2>Tnp transposon insertion in an open reading frame of unknown function (ncr) in Acinetobacter baumannii resulted in an 8-fold increase in ciprofloxacin resistance (Cip(r)). Transposon insertions in an ncr mutant that reduced Cip(r) back to wild type mapped to three genes encoding subunits of the RecCBD exonuclease. The ncr mutation increased transcription of the recCBD genes, and overexpression of the recCBD genes in a wild-type background resulted in a 4-fold increase in Cip(r).
Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia, USA.
Sunil D
SD
Saroj
Katy M
KM
Clemmer
Robert A
RA
Bonomo
Philip N
PN
Rather
D040981:Acinetobacter baumannii / Q000187:drug effects / Q000235:genetics*; D004251:DNA Transposable Elements; D024901:Drug Resistance, Multiple, Bacterial / Q000187:drug effects / Q000235:genetics*; D043211:Exodeoxyribonuclease V / Q000235:genetics*; D024841:Fluoroquinolones / Q000494:pharmacology*; D015870:Gene Expression; D015723:Gene Library; D005798:Genes, Bacterial; D005818:Genetic Engineering; D008826:Microbial Sensitivity Tests; D009154:Mutation; D016366:Open Reading Frames; D021122:Protein Subunits / Q000235:genetics
D004251:DNA Transposable Elements; D024841:Fluoroquinolones; D021122:Protein Subunits; D043211:Exodeoxyribonuclease V