Evidence map›Paper›PMID 42328795›Full record

ArticleNucleic acids research2026

Exploring the genetic landscape of ciprofloxacin-induced DNA supercompaction in Escherichia coli.

Krister Vikedal, Natalia Berges, Ida Mathilde Marstein Riisnæs, Synnøve Brandt Ræder, Jørgen Vildershøj Bjørnholt, Magnar Bjørås, Kirsten Skarstad, Emily Helgesen, James Alexander Booth

Abstract read
In one paragraph

Article in Nucleic acids research, 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

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

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

9 authors.

Krister VikedalDepartment of Microbiology, Oslo University Hospital, Rikshospitalet, 0373 Oslo, Norway.ORCID 0000-0002-7475-4636
Natalia BergesDepartment of Microbiology, Oslo University Hospital, Rikshospitalet, 0373 Oslo, Norway.ORCID 0009-0007-1357-2154
Ida Mathilde Marstein RiisnæsDepartment of Microbiology, Oslo University Hospital, Rikshospitalet, 0373 Oslo, Norway.
Synnøve Brandt RæderDepartment of Microbiology, Oslo University Hospital, Rikshospitalet, 0373 Oslo, Norway.ORCID 0000-0002-1562-6343
Jørgen Vildershøj BjørnholtDepartment of Microbiology, Oslo University Hospital, Rikshospitalet, 0373 Oslo, Norway.ORCID 0000-0002-0079-8062
Magnar BjøråsDepartment of Microbiology, Oslo University Hospital, Rikshospitalet, 0373 Oslo, Norway.ORCID 0000-0001-8759-1170
Kirsten SkarstadDepartment of Microbiology, Oslo University Hospital, Rikshospitalet, 0373 Oslo, Norway.ORCID 0000-0002-8563-2730
Emily HelgesenDepartment of Microbiology, Oslo University Hospital, Rikshospitalet, 0373 Oslo, Norway.ORCID 0000-0002-3992-7394
James Alexander BoothDepartment of Microbiology, Oslo University Hospital, Rikshospitalet, 0373 Oslo, Norway.ORCID 0000-0001-9452-3424

Funding

Helse Sør-Øst RHF 2019022Helse Sør-Øst RHF 2020043Norwegian Surveillance Program for Antimicrobial Resistance 2024-04
6 · The paper itself

Abstract

DNA-damaging antibiotics like ciprofloxacin (CIP) induce extensive double-strand breaks in Escherichia coli, triggering both the SOS response and rapid DNA supercompaction. To uncover genes involved in the latter process beyond the previously identified key orchestrators encoded by recN and recA, we developed a novel machine learning-assisted high-throughput screening workflow and applied it to nearly 4000 E. coli strains, including the Keio collection's single-gene deletion strains and additional in-house strains. Conservative validation identified 15 hit strains with impaired DNA supercompaction. While defects in recombinational repair genes were associated with the most severe impairments, our investigation also revealed genes not previously associated with DNA compaction or repair that had milder and more heterogeneous effects on supercompaction, including yaiW, which encodes a membrane-associated protein. Notably, several non-DNA-repair gene deletions affected RecN colocalization with the nucleoid, recN expression, SOS response activity, or survival after CIP exposure, supporting indirect or modulatory roles. Altogether, this work confirms RecN and RecA as primary drivers of DNA supercompaction and demonstrates that high-content imaging combined with machine learning-assisted analysis provides a scalable approach to explore bacterial DNA organization phenotypes and DNA damage responses.

Indexed as

Anti-Bacterial AgentsCiprofloxacinDNA, BacterialEscherichia coliDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA RepairEscherichia coli ProteinsExodeoxyribonuclease VGene DeletionMachine LearningRec A RecombinasesSOS Response, GeneticsAnti-Bacterial AgentsCiprofloxacinDNA, BacterialDNA-Binding ProteinsEscherichia coli ProteinsExodeoxyribonuclease VrecA protein, E coliRec A Recombinases

Identifiers

PMID42328795
PMCPMC13284718

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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.