Evidence map›Paper›PMID 41781441›Full record

ArticleScientific reports2026

Exploring molecular mechanisms of aminoglycoside resistance in Escherichia coli MG1655 using the antibiotic resistance growth plate.

L B L Cullen, C J L Eldridge, B P Jones, G Forster-Wilkins, S P Lawton, M D Fielder

Abstract read
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

L B L CullenSchool of Life Sciences, Kingston University London, Kingston Upon-Thames, London, KT1 2EE, UK.
C J L EldridgeSchool of Life Sciences, Kingston University London, Kingston Upon-Thames, London, KT1 2EE, UK.
B P JonesSchool of Life Sciences, Kingston University London, Kingston Upon-Thames, London, KT1 2EE, UK.
G Forster-WilkinsSchool of Life Sciences, Kingston University London, Kingston Upon-Thames, London, KT1 2EE, UK.
S P LawtonCentre for Epidemiology and Planetary Health, SRUC School of Veterinary Medicine, Scotland's Rural College, West Mains Road, Edinburgh, EH9 3JG, UK.
M D FielderSchool of Life Sciences, Kingston University London, Kingston Upon-Thames, London, KT1 2EE, UK. m.fielder@kingston.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The overuse of antibiotics in human and animal health has driven the rapid emergence of multi-drug-resistant bacterial strains. To investigate the molecular mechanisms underlying resistance, we developed the Antibiotic Resistance Growth Plate (ARGP), an experimental evolution tool that imposes a spatiotemporal antibiotic gradient. Using the ARGP, Escherichia coli MG1655 populations developed resistance to gentamicin up to 10x MIC within two days. Whole-genome sequencing of wildtype and resistant strains revealed mutations in 16 S rRNA genes and the fusA gene. Bioinformatic, phylogenetic, and molecular docking analyses were used to demonstrate the mechanical significance of the fusA gene in the molecular pathways of gentamicin resistance in E. coli MG1655, where mutations in fusA alter EF-G function, disrupting gentamicin's inhibition of ribosomal translocation. These results highlight the rapidity and specificity of adaptive responses to aminoglycosides and establish the ARGP as a versatile tool for studying the molecular pathways driving antibiotic resistance.

Indexed as

AminoglycosidesAnti-Bacterial AgentsDrug Resistance, BacterialEscherichia coliEscherichia coli ProteinsGentamicinsMicrobial Sensitivity TestsMolecular Docking SimulationMutationPhylogenyRNA, Ribosomal, 16SAminoglycosidesAnti-Bacterial AgentsEscherichia coli ProteinsGentamicinsRNA, Ribosomal, 16S

Identifiers

PMID41781441
PMCPMC13068909

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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.