Evidence map›Paper›PMID 40631979›Full record

ArticleeLife2025

Fast evolution of SOS-independent multi-drug resistance in bacteria.

Le Zhang, Yunpeng Guan, YuenYee Cheng, Nural N Cokcetin, Amy L Bottomley, Andrew Robinson, Elizabeth J Harry, Antoine M van Oijen, Qian Peter Su, Dayong Jin

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in eLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

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

4 citing papers in PubMed.

  1. Review
  2. Antibiotic Resistance inAntibiotics (Basel, Switzerland) · 2026
    Review
  3. Article
  4. Antibiotic resistance mediated by gene amplifications.npj antimicrobials and resistance · 2024
    Review
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

10 authors.

Le Zhang *Institute for Biomedical Materials and Devices (IBMD), University of Technology Sydney, Ultimo, Australia.ORCID https://orcid.org/0000-0003-0641-2383
Yunpeng Guan *Institute for Biomedical Materials and Devices (IBMD), University of Technology Sydney, Ultimo, Australia.
YuenYee ChengInstitute for Biomedical Materials and Devices (IBMD), University of Technology Sydney, Ultimo, Australia.
Nural N CokcetinAustralian Institute for Microbiology & Infection (AIMI), University of Technology Sydney, Ultimo, Australia.
Amy L BottomleyAustralian Institute for Microbiology & Infection (AIMI), University of Technology Sydney, Ultimo, Australia.
Andrew RobinsonSchool of Chemistry and Molecular Bioscience, University of Wollongong, Wollongong, Australia.ORCID https://orcid.org/0000-0002-3544-0976
Elizabeth J HarryAustralian Institute for Microbiology & Infection (AIMI), University of Technology Sydney, Ultimo, Australia.
Antoine M van OijenSchool of Chemistry and Molecular Bioscience, University of Wollongong, Wollongong, Australia.ORCID https://orcid.org/0000-0002-1794-5161
Qian Peter SuInstitute for Biomedical Materials and Devices (IBMD), University of Technology Sydney, Ultimo, Australia.ORCID https://orcid.org/0000-0001-7364-3945
Dayong JinInstitute for Biomedical Materials and Devices (IBMD), University of Technology Sydney, Ultimo, Australia.ORCID https://orcid.org/0000-0003-1046-2666

Funding

Australia China Science and Research SQ2017YFGH001190Australian Research Council ACSRF658277Australian Research Council APP1165135National Health and Medical Research Council APP1177374Science and technology innovation commission of shen zhen KQTD20170810110913065
6 · The paper itself

Abstract

The killing mechanism of many antibiotics involves the induction of DNA damage, either directly or indirectly, which activates the SOS response. RecA, the master regulator of the SOS response, has been shown to play a central role in the evolution of resistance to fluoroquinolones, even after short-term exposure. While this paradigm is well established for DNA-damaging antibiotics, it remains unclear whether β-lactams elicit similar resistance dynamics or depend on RecA and SOS-mediated mechanisms. In this study, we observed a rapid and stable evolution of β-lactam resistance (20-fold MIC increase within 8 hr) in

Indexed as

Anti-Bacterial AgentsDrug Resistance, Multiple, BacterialEscherichia coliEvolution, MolecularSOS Response, GeneticsAmpicillinDNA-Binding ProteinsDNA RepairEscherichia coli ProteinsMicrobial Sensitivity TestsMutationReactive Oxygen SpeciesRec A RecombinasesAmpicillinAnti-Bacterial AgentsDNA-Binding ProteinsEscherichia coli ProteinsReactive Oxygen SpeciesrecA protein, E coliRec A Recombinasesantibiotic resistanceDNA repairE. colievolutioninfectious diseasemicrobiologymutationselection

Identifiers

PMID40631979
PMCPMC12240585

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.