Open AccessRole of an acrR mutation in multidrug resistance of in vitro ‐selected fluoroquinolone‐resistant mutants of Salmonella enterica serovar Typhimurium
Author(s) -
Olliver Anne,
Vallé Michel,
ChaslusDancla Elisabeth,
Cloeckaert Axel
Publication year - 2004
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2004.tb09766.x
Subject(s) - salmonella enterica , efflux , dna gyrase , mutant , biology , microbiology and biotechnology , mutation , salmonella , multiple drug resistance , topoisomerase iv , complementation , quinolone , escherichia coli , genetics , gene , drug resistance , antibiotics , bacteria
Quinolone resistance in Salmonella spp. is usually attributed to both active efflux and mutations leading to modification of the target enzymes DNA gyrase and topoisomerase IV. Here, we investigated the presence of mutations in the efflux regulatory genes of fluoroquinolone‐ and multidrug‐resistant mutants of Salmonella enterica serovar Typhimurium ( S. Typhimurium) selected in vitro with enrofloxacin that both carried a mutation in the target gene gyrA and overproduced the AcrAB efflux pump. No mutations were detected in the global regulatory loci marRAB and soxRS for the four strains studied. A mutation in acrR , the local repressor of acrAB , was found for two ciprofloxacin‐resistant selected‐mutants, leading to duplication of amino acids Ile75 and Glu76. Complementation experiments with wild‐type acrR showed that the mutation identified in acrR partially contributed to the increase in resistance levels to several unrelated antibiotics. The acrR mutation also contributed to acrAB overexpression as shown by RT‐PCR. Thus, this study underlines the role of an acrR mutation, in addition to the mutation in gyrA , in the fluoroquinolone and multidrug resistance phenotype of S. Typhimurium mutants, through overexpression of acrAB.