ArticleThe Journal of antimicrobial chemotherapy2013
Genetic inactivation of acrAB or inhibition of efflux induces expression of ramA.
Article in The Journal of antimicrobial chemotherapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 53 citations in OpenAlex.
- How resistance-nodulation-division (RND) efflux pumps contribute to virulence.PLoS pathogens · 2026Review
- A specific amount of RamA must be reached to trigger increased expression of AcrAB, enhance efflux, and confer multidrug resistance.Nucleic acids research · 2026Article
- Metabolism-dependent succinylation governs resource allocation for antibiotic resistance.Science advances · 2025Article
- Extending the Potency and Lifespan of Antibiotics: Inhibitors of Gram-Negative Bacterial Efflux Pumps.ACS infectious diseases · 2024Review
- Article
- Drug resistance and physiological roles of RND multidrug efflux pumps inMicrobiology (Reading, England) · 2023Article
- Contribution of the efflux pump AcrAB-TolC to the tolerance of chlorhexidine and other biocides inJournal of medical microbiology · 2022Article
- Dynamic Boolean modelling reveals the influence of energy supply on bacterial efflux pump expression.Journal of the Royal Society, Interface · 2022Article
- A palette of fluorophores that are differentially accumulated by wild-type and mutant strains ofMicrobiology (Reading, England) · 2021Article
- Article
- Chlorpromazine and Amitriptyline Are Substrates and Inhibitors of the AcrB Multidrug Efflux Pump.mBio · 2020Article
- Involvement of multiple influx and efflux transporters in the accumulation of cationic fluorescent dyes by Escherichia coli.BMC microbiology · 2019Article
- Flow Cytometric Analysis of Efflux by Dye Accumulation.Frontiers in microbiology · 2019Article
- Exposure to Sub-inhibitory Concentrations of the Chemosensitizer 1-(1-Naphthylmethyl)-Piperazine Creates Membrane Destabilization in Multi-Drug ResistantFrontiers in microbiology · 2019Article
- CsrA maximizes expression of the AcrAB multidrug resistance transporter.Nucleic acids research · 2017Article
- Article
- RpoE is a Putative Antibiotic Resistance Regulator of Salmonella enteric Serovar Typhi.Current microbiology · 2016Article
- The challenge of efflux-mediated antibiotic resistance in Gram-negative bacteria.Clinical microbiology reviews · 2015Review
- AcrB drug-binding pocket substitution confers clinically relevant resistance and altered substrate specificity.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Expression of homologous RND efflux pump genes is dependent upon AcrB expression: implications for efflux and virulence inhibitor design.The Journal of antimicrobial chemotherapy · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectivesThe transcriptional activator RamA regulates production of the multidrug resistance efflux AcrAB-TolC system in several Enterobacteriaceae. This study investigated factors that lead to increased expression of ramA.
methodsIn order to monitor changes in ramA expression, the promoter region of ramA was fused to a gfp gene encoding an unstable green fluorescence protein (GFP) on the reporter plasmid, pMW82. The ramA reporter plasmid was transformed into Salmonella Typhimurium SL1344 and a ΔacrB mutant. The response of the reporter to subinhibitory concentrations of antibiotics, dyes, biocides, psychotropic agents and efflux inhibitors was measured during growth over a 5 h time period.
resultsOur data revealed that the expression of ramA was increased in a ΔacrB mutant and also in the presence of the efflux inhibitors phenylalanine-arginine-β-naphthylamide, carbonyl cyanide m-chlorophenylhydrazone and 1-(1-naphthylmethyl)-piperazine. The phenothiazines chlorpromazine and thioridazine also increased ramA expression, triggering the greatest increase in GFP expression. However, inducers of Escherichia coli marA and soxS and 12 of 17 tested antibiotic substrates of AcrAB-TolC did not induce ramA expression.
conclusionsThis study shows that expression of ramA is not induced by most substrates of the AcrAB-TolC efflux system, but is increased by mutational inactivation of acrB or when efflux is inhibited.
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