Evidence map›Paper›PMID 24043404›Full record

ArticleThe Journal of antimicrobial chemotherapy2014

Regulation of acrAB expression by cellular metabolites in Escherichia coli.

Cristian Ruiz, Stuart B Levy

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of antimicrobial chemotherapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Carbapenem-ResistantAntibiotics (Basel, Switzerland) · 2026
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  4. Characterization of anAntibiotics (Basel, Switzerland) · 2026
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  6. Antibiotic resistance inFrontiers in microbiology · 2026
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  10. Disruption of the EmrAB-TolC efflux pump ofmicroPublication biology · 2025
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  11. The complex development of psoralen-interstrand crosslink resistance inbioRxiv : the preprint server for biology · 2024
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  12. Dual role ofiMetaOmics · 2024
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  14. Review
  15. Fitness trade-offs of multidrug efflux pumps inApplied and environmental microbiology · 2024
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  17. The induced and intrinsic resistance ofMicrobiology spectrum · 2024
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  18. Article
  19. Article
  20. Article

9 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Cristian RuizCenter for Adaptation Genetics and Drug Resistance and the Department of Molecular Biology and Microbiology, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA, USA.
Stuart B Levy
Tufts University · US

Funding

The multiple antibiotic resistance (MAR)regulonR01AI056021 · NIAID · TUFTS UNIVERSITY BOSTON · PI LEVY, STUART B. · 2003 to 2017
$8.9M
NIAID NIH HHS AI56021NIAID NIH HHS R01 AI056021
6 · The paper itself

Abstract

objectivesMultidrug efflux pumps mediate resistance to antibiotics and other toxic compounds. We studied the role of AcrAB-TolC, the main efflux pump in Escherichia coli, in regulating gene expression.

methodsDeletion mutants, an acrABp-lacZ fusion and reverse transcription-real-time quantitative PCR experiments were used to study the role of AcrAB-TolC and metabolism in regulating gene expression of the acrAB operon and its transcriptional regulators.

resultsDeletion of the acrB gene increased the expression of the acrAB operon. A similar induction of acrAB was found when acrA or tolC was deleted, and when the pump function was inhibited using phenylalanine-arginine-β-naphthylamide. The induction of acrAB in the ΔacrB strain was totally (AcrR or SoxS) or partially (SoxR or MarA) prevented when the genes for these acrAB regulators were also deleted. The expression of soxS and marA, but not of acrR, was increased in the ΔacrB strain, which also showed altered expression of many other genes related to different cellular processes, including motility. Deletion of the metabolic genes entA and entE (enterobactin biosysnthesis), glpX (gluconeogenesis), cysH (cysteine biosynthesis) and purA (purine biosynthesis) also prevented activation of the acrAB promoter in the ΔacrB strain. Addition of the enterobactin biosynthesis intermediate metabolite 2,3-dihydroxybenzoate induced the expression of acrAB.

conclusionsThese results together suggest a model in which the AcrAB-TolC pump effluxes cellular metabolites that are toxic and/or have a signalling role. If the pump is inactivated or inhibited, these metabolites would accumulate, inactivating AcrR and/or up-regulating soxS and marA expression, ultimately triggering the up-regulation of acrAB expression to restore homeostasis.

Indexed as

Gene Expression Regulation, BacterialATP-Binding Cassette, Sub-Family C ProteinsCells, CulturedCellular MicroenvironmentEnergy MetabolismEscherichia coliEscherichia coli ProteinsOperonSignal TransductionAcrB protein, E coliATP-Binding Cassette, Sub-Family C ProteinsEscherichia coli ProteinsAcrAB-TolCacrRgene regulationmarAmultidrug effluxsoxS

Identifiers

PMID24043404
PMCPMC3886929
OpenAlexW2138214676

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.