Related Experiment Videos
RobA-induced multiple antibiotic resistance largely depends on the activation of the AcrAB efflux
T Tanaka1, T Horii, K Shibayama
1Department of Bacteriology, Nagoya University School of Medicine, Aichi, Japan.
Abstract:
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.
Insights
Overexpression of RobA induces antibiotic resistance in Escherichia coli by activating AcrAB efflux and micF. This resistance mechanism is independent of OmpF porin expression.
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- RobA, a DNA-binding protein from the XylS/AraC family, is known to induce multiple antibiotic resistance when overexpressed in Escherichia coli.
- Understanding the mechanisms behind antibiotic resistance is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role of RobA in inducing multiple antibiotic resistance in Escherichia coli.
- To determine the dependence of RobA-induced resistance on OmpF porin and the AcrAB efflux system.
Main Methods:
- Introduction of a multicopy robA plasmid (pMEP1) into OmpF mutants and an AcrAB-deficient mutant.
- Assessment of antibiotic susceptibility in engineered Escherichia coli strains.
Main Results:
- RobA-induced multi-drug resistance in OmpF mutants was independent of OmpF porin expression.
- A delta ompF mutant (TK007) exhibited increased sensitivity to antibiotics upon pMEP1 introduction.
- RobA had no observable effect on multi-drug resistance induction in an acrA1- mutant.
Conclusions:
- The multiple antibiotic resistance induced by RobA overexpression is primarily mediated by the activation of the AcrAB efflux pump.
- Activation of micF also contributes to the RobA-mediated antibiotic resistance phenotype.