Evidence map›Paper›PMID 28262707›Full record

ArticleNature communications2017

Management of E. coli sister chromatid cohesion in response to genotoxic stress.

Elise Vickridge, Charlene Planchenault, Charlotte Cockram, Isabel Garcia Junceda, Olivier Espéli

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 57 citations in OpenAlex.

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  6. Purification and In Vitro Analysis of Escherichia coli RecN.Methods in molecular biology (Clifton, N.J.) · 2026
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  9. Comparative Genomic Analysis Reveals Key Changes in the Genome ofInternational journal of molecular sciences · 2024
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  15. SMC protein RecN drives RecA filament translocation for in vivo homology search.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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

5 authors at 1 institution in 1 country.

Elise VickridgeCenter for Interdisciplinary Research in Biology (CIRB), Collège de France, UMR CNRS-7241, INSERM U1050, PSL Research University, 11 place Marcelin Berthelot, 75005 Paris, France.
Charlene PlanchenaultCenter for Interdisciplinary Research in Biology (CIRB), Collège de France, UMR CNRS-7241, INSERM U1050, PSL Research University, 11 place Marcelin Berthelot, 75005 Paris, France.
Charlotte CockramCenter for Interdisciplinary Research in Biology (CIRB), Collège de France, UMR CNRS-7241, INSERM U1050, PSL Research University, 11 place Marcelin Berthelot, 75005 Paris, France.
Isabel Garcia JuncedaCenter for Interdisciplinary Research in Biology (CIRB), Collège de France, UMR CNRS-7241, INSERM U1050, PSL Research University, 11 place Marcelin Berthelot, 75005 Paris, France.
Olivier EspéliCenter for Interdisciplinary Research in Biology (CIRB), Collège de France, UMR CNRS-7241, INSERM U1050, PSL Research University, 11 place Marcelin Berthelot, 75005 Paris, France.
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant DNA replication is a major source of the mutations and chromosomal rearrangements associated with pathological disorders. In bacteria, several different DNA lesions are repaired by homologous recombination, a process that involves sister chromatid pairing. Previous work in Escherichia coli has demonstrated that sister chromatid interactions (SCIs) mediated by topological links termed precatenanes, are controlled by topoisomerase IV. In the present work, we demonstrate that during the repair of mitomycin C-induced lesions, topological links are rapidly substituted by an SOS-induced sister chromatid cohesion process involving the RecN protein. The loss of SCIs and viability defects observed in the absence of RecN were compensated by alterations in topoisomerase IV, suggesting that the main role of RecN during DNA repair is to promote contacts between sister chromatids. RecN also modulates whole chromosome organization and RecA dynamics suggesting that SCIs significantly contribute to the repair of DNA double-strand breaks (DSBs).

Indexed as

Bacterial ProteinsChromatidsChromosome SegregationDNA, BacterialDNA Breaks, Double-StrandedDNA DamageDNA ReplicationDNA Restriction EnzymesDNA Topoisomerase IVEscherichia coliMitomycinRec A RecombinasesSister Chromatid ExchangeSOS Response, GeneticsBacterial ProteinsDNA, BacterialDNA Restriction EnzymesDNA Topoisomerase IVMitomycinRec A RecombinasesRecN protein, Bacteria

Identifiers

PMID28262707
PMCPMC5343486
OpenAlexW2594215657

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.