Evidence map›Paper›PMID 30862812›Full record

ArticleNature communications2019

Enhanced antibiotic resistance development from fluoroquinolone persisters after a single exposure to antibiotic.

Theresa C Barrett, Wendy W K Mok, Allison M Murawski, Mark P Brynildsen

Abstract readVideo-Audio Media
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.

0numbers the graph read from it
0cells of the map it votes in
126citing 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

126 citing papers in PubMed.

  1. Review
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  10. Glycerol-Driven Energy and Proteostasis Underpin Antibiotic Tolerance inbioRxiv : the preprint server for biology · 2026
    Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Sensitivity profile of tolerant and persistent Staphylococcus spp. from goat mastitis to Jatobá (Hymenaea martiana Hayne) extract.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2026
    Article
  17. Article
  18. Stationary-phasemSphere · 2026
    Article
  19. Article
  20. Article

66 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

4 authors.

Theresa C BarrettDepartment of Molecular Biology, Princeton University, Princeton, NJ, 08544, USA.
Wendy W K MokDepartment of Chemical and Biological Engineering, Princeton University, Princeton, NJ, 08544, USA.
Allison M MurawskiDepartment of Molecular Biology, Princeton University, Princeton, NJ, 08544, USA.
Mark P BrynildsenDepartment of Molecular Biology, Princeton University, Princeton, NJ, 08544, USA. mbrynild@princeton.edu.

Funding

Examining fluoroquinolone-induced DNA damage in persisters and its contributions to antibiotic resistance.R01AI130293 · NIAID · PRINCETON UNIVERSITY · PI BRYNILDSEN, MARK P · 2017 to 2021
$2.0M
Exploring Persister Antibiotic Responses as a Source of Biomarkers and Elimination StrategiesR21AI115075 · NIAID · PRINCETON UNIVERSITY · PI BRYNILDSEN, MARK P · 2015 to 2016
$446k
Development of a method to rapidly quantify persister gene expressionF30AI114163 · NIAID · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI BARRETT, THERESA · 2014 to 2018
$238k
NIAID NIH HHS F30 AI114163NIAID NIH HHS R01 AI130293NIAID NIH HHS R21 AI115075NIH HHS F30AI114163NIH HHS R01AI130293NIH HHS R21AI115075
6 · The paper itself

Abstract

Bacterial persisters are able to tolerate high levels of antibiotics and give rise to new populations. Persister tolerance is generally attributed to minimally active cellular processes that prevent antibiotic-induced damage, which has led to the supposition that persister offspring give rise to antibiotic-resistant mutants at comparable rates to normal cells. Using time-lapse microscopy to monitor Escherichia coli populations following ofloxacin treatment, we find that persisters filament extensively and induce impressive SOS responses before returning to a normal appearance. Further, populations derived from fluoroquinolone persisters contain significantly greater quantities of antibiotic-resistant mutants than those from untreated controls. We confirm that resistance is heritable and that the enhancement requires RecA, SOS induction, an opportunity to recover from treatment, and the involvement of error-prone DNA polymerase V (UmuDC). These findings show that fluoroquinolones damage DNA in persisters and that the ensuing SOS response accelerates the development of antibiotic resistance from these survivors.

Indexed as

Anti-Bacterial AgentsDNA DamageDNA-Directed DNA PolymeraseDrug Resistance, BacterialEscherichia coliEscherichia coli ProteinsMicroscopy, FluorescenceOfloxacinRec A RecombinasesSOS Response, GeneticsTime-Lapse ImagingAnti-Bacterial AgentsDNA-Directed DNA PolymeraseDNA polymerase V, E coliEscherichia coli ProteinsOfloxacinRec A Recombinases

Identifiers

PMID30862812
PMCPMC6414640

What OpenQuestion holds

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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.