Tanaka T, Horii T, Shibayama K, Sato K, Ohsuka S, Arakawa Y, Yamaki K, Takagi K, Ohta M
Department of Bacteriology, Nagoya University School of Medicine, Aichi, Japan.
Microbiol Immunol. 1997;41(9):697-702. doi: 10.1111/j.1348-0421.1997.tb01913.x.
RobA is a member of the XylS/AraC subfamily of DNA binding proteins, and when overexpressed, it induces multiple antibiotic resistance in Escherichia coli. In this study, we introduced a multicopy robA plasmid (pMEP1) and its derivative into OmpF mutants and an AcrAB-deficient mutant. We found that a decrease in susceptibility to multiple antibiotics in these OmpF mutants when pMEP1 was introduced did not depend on OmpF porin expression. Interestingly, a delta ompF mutant (TK007) became more sensitive when pMEP1 was introduced. Moreover, no effect of RobA on the induction of multiple antibiotic resistance in an acrA1- mutant was observed. Therefore, we conclude that the multiple antibiotic resistance induced by the overexpression of RobA largely depends on the activation of the AcrAB efflux, as well as the activation of micF.
RobA是DNA结合蛋白XylS/AraC亚家族的成员,过表达时会在大肠杆菌中诱导多重抗生素耐药性。在本研究中,我们将多拷贝robA质粒(pMEP1)及其衍生物导入OmpF突变体和AcrAB缺陷突变体中。我们发现,导入pMEP1时,这些OmpF突变体对多种抗生素的敏感性降低并不依赖于OmpF孔蛋白的表达。有趣的是,导入pMEP1时,ΔompF突变体(TK007)变得更加敏感。此外,未观察到RobA对acrA1 - 突变体中多重抗生素耐药性诱导的影响。因此,我们得出结论,RobA过表达诱导的多重抗生素耐药性很大程度上取决于AcrAB外排的激活以及micF的激活。