Evidence map›Paper›PMID 39572529›Full record

ArticleNature communications2024

Genome-wide profiling of DNA repair proteins in single cells.

Kim L de Luca, Pim M J Rullens, Magdalena A Karpinska, Sandra S de Vries, Agnieszka Gacek-Matthews, Lőrinc S Pongor, Gaëlle Legube, Joanna W Jachowicz, A Marieke Oudelaar, Jop Kind

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

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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

10 authors.

Kim L de Luca *Hubrecht Institute, Royal Netherlands Academy of Arts and Sciences (KNAW) & University Medical Center Utrecht, Utrecht, the Netherlands. science@kimdeluca.com.ORCID 0000-0002-5900-5100
Pim M J Rullens *Hubrecht Institute, Royal Netherlands Academy of Arts and Sciences (KNAW) & University Medical Center Utrecht, Utrecht, the Netherlands.ORCID 0009-0007-4176-5674
Magdalena A KarpinskaGenome Organization and Regulation, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany.ORCID 0000-0002-1516-2083
Sandra S de VriesHubrecht Institute, Royal Netherlands Academy of Arts and Sciences (KNAW) & University Medical Center Utrecht, Utrecht, the Netherlands.
Agnieszka Gacek-MatthewsInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna Biocenter (VBC), Vienna, Austria.ORCID 0000-0001-5884-583X
Lőrinc S PongorCancer Genomics and Epigenetics Core Group, Hungarian Center of Excellence for Molecular Medicine (HCEMM), Szeged, Hungary.ORCID 0000-0001-5917-4628
Gaëlle LegubeMCD, Centre de Biologie Intégrative (CBI), CNRS, Université de Toulouse, Toulouse, France.ORCID 0000-0002-4784-2702
Joanna W JachowiczInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna Biocenter (VBC), Vienna, Austria.ORCID 0000-0002-1599-682X
A Marieke OudelaarGenome Organization and Regulation, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany.ORCID 0000-0002-4016-6158
Jop KindHubrecht Institute, Royal Netherlands Academy of Arts and Sciences (KNAW) & University Medical Center Utrecht, Utrecht, the Netherlands. j.kind@hubrecht.eu.ORCID 0000-0001-7538-2638

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accurate repair of DNA damage is critical for maintenance of genomic integrity and cellular viability. Because damage occurs non-uniformly across the genome, single-cell resolution is required for proper interrogation, but sensitive detection has remained challenging. Here, we present a comprehensive analysis of repair protein localization in single human cells using DamID and ChIC sequencing techniques. This study reports genome-wide binding profiles in response to DNA double-strand breaks induced by AsiSI, and explores variability in genomic damage locations and associated repair features in the context of spatial genome organization. By unbiasedly detecting repair factor localization, we find that repair proteins often occupy entire topologically associating domains, mimicking variability in chromatin loop anchoring. Moreover, we demonstrate the formation of multi-way chromatin hubs in response to DNA damage. Notably, larger hubs show increased coordination of repair protein binding, suggesting a preference for cooperative repair mechanisms. Together, our work offers insights into the heterogeneous processes underlying genome stability in single cells.

Indexed as

ChromatinDNA Breaks, Double-StrandedDNA RepairSingle-Cell AnalysisDNA-Binding ProteinsDNA DamageGenome, HumanGenomic InstabilityHumansProtein BindingChromatinDNA-Binding Proteins

Identifiers

PMID39572529
PMCPMC11582664

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.