Evidence map›Paper›PMID 37898641›Full record

ArticleNature communications2023

The chromatin network helps prevent cancer-associated mutagenesis at transcription-replication conflicts.

Aleix Bayona-Feliu, Emilia Herrera-Moyano, Nibal Badra-Fajardo, Iván Galván-Femenía, María Eugenia Soler-Oliva, Andrés Aguilera

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

36 citing papers in PubMed, 46 citations in OpenAlex.

  1. Chromatin Packing Domain Engineering Through the Manipulation of Nuclear Cationic States.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  14. Deaminase Modulation Driving a New Era in Drug Development.International journal of molecular sciences · 2025
    Review
  15. Article
  16. Review
  17. Transcription-Replication Conflicts: Unlocking New Frontiers in Cancer.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  18. Review
  19. Article
  20. Article
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

6 authors at 2 institutions in 1 country.

Aleix Bayona-FeliuCentro Andaluz de Biología Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla-CSIC-Universidad Pablo de Olavide, 41092, Seville, Spain. aleix.bayona@irbbarcelona.org.ORCID 0000-0002-7412-1652
Emilia Herrera-MoyanoCentro Andaluz de Biología Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla-CSIC-Universidad Pablo de Olavide, 41092, Seville, Spain.ORCID 0000-0003-3948-3874
Nibal Badra-FajardoCentro Andaluz de Biología Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla-CSIC-Universidad Pablo de Olavide, 41092, Seville, Spain.
Iván Galván-FemeníaInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.
María Eugenia Soler-OlivaCentro Andaluz de Biología Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla-CSIC-Universidad Pablo de Olavide, 41092, Seville, Spain.ORCID 0000-0002-1881-1720
Andrés AguileraCentro Andaluz de Biología Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla-CSIC-Universidad Pablo de Olavide, 41092, Seville, Spain. aguilo@us.es.ORCID 0000-0003-4782-1714
Centro Andaluz de Biología Molecular y Medicina Regenerativa · ESInstitute for Research in Biomedicine · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome instability is a feature of cancer cells, transcription being an important source of DNA damage. This is in large part associated with R-loops, which hamper replication, especially at head-on transcription-replication conflicts (TRCs). Here we show that TRCs trigger a DNA Damage Response (DDR) involving the chromatin network to prevent genome instability. Depletion of the key chromatin factors INO80, SMARCA5 and MTA2 results in TRCs, fork stalling and R-loop-mediated DNA damage which mostly accumulates at S/G2, while histone H3 Ser10 phosphorylation, a mark of chromatin compaction, is enriched at TRCs. Strikingly, TRC regions show increased mutagenesis in cancer cells with signatures of homologous recombination deficiency, transcription-coupled nucleotide excision repair (TC-NER) and of the AID/APOBEC cytidine deaminases, being predominant at head-on collisions. Thus, our results support that the chromatin network prevents R-loops and TRCs from genomic instability and mutagenic signatures frequently associated with cancer.

Indexed as

ChromatinNeoplasmsDNA DamageDNA ReplicationGenomic InstabilityHistone DeacetylasesHumansMutagenesisRepressor ProteinsTranscription, GeneticChromatinHistone DeacetylasesMTA2 protein, humanRepressor Proteins

Identifiers

PMID37898641
PMCPMC10613258
OpenAlexW4387997345

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.