Evidence map›Paper›PMID 39984484›Full record

ArticleNature communications2025

EccDNA atlas in male mice reveals features protecting genes against transcription-induced eccDNA formation.

Xue Liang, Gerard Arrey, Yating Qin, Lucía Álvarez-González, Judith Mary Hariprakash, Jie Ma, Sylvester Holt, Peng Han, Yonglun Luo, Hanbo Li and 3 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
  2. Article
  3. Functional role of small extrachromosomal circular DNA in colorectal cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Extrachromosomal Circular DNA and Transposable Elements in Type 2 Diabetes.International journal of molecular sciences · 2025
    Review
  10. 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

13 authors.

Xue Liang *Section for Ecology and Evolution, Department of Biology, University of Copenhagen, Copenhagen, Denmark.
Gerard Arrey *Section for Ecology and Evolution, Department of Biology, University of Copenhagen, Copenhagen, Denmark.
Yating QinSection for Ecology and Evolution, Department of Biology, University of Copenhagen, Copenhagen, Denmark.
Lucía Álvarez-GonzálezDepartament de Biologia Cel·lular, Fisiologia i Immunologia, Universitat Autònoma de Barcelona, Cerdanyola del Vallès, Spain.ORCID http://orcid.org/0000-0001-8154-8614
Judith Mary HariprakashSection for Ecology and Evolution, Department of Biology, University of Copenhagen, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-1164-347X
Jie MaLars Bolund Institute of Regenerative Medicine, Qingdao-Europe Advanced Institute for Life Sciences, BGI Research, Qingdao, 266555, China.
Sylvester HoltSection for Ecology and Evolution, Department of Biology, University of Copenhagen, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-9958-0169
Peng HanSection for Ecology and Evolution, Department of Biology, University of Copenhagen, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-3405-087X
Yonglun LuoDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.ORCID http://orcid.org/0000-0002-0007-7759
Hanbo LiLars Bolund Institute of Regenerative Medicine, Qingdao-Europe Advanced Institute for Life Sciences, BGI Research, Qingdao, 266555, China.ORCID http://orcid.org/0000-0001-8778-9988
Aurora Ruiz-HerreraDepartament de Biologia Cel·lular, Fisiologia i Immunologia, Universitat Autònoma de Barcelona, Cerdanyola del Vallès, Spain.ORCID http://orcid.org/0000-0003-3868-6151
Henriette PilegaardSection for Cell Biology and Physiology, Department of Biology, University of Copenhagen, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-1071-0327
Birgitte RegenbergSection for Ecology and Evolution, Department of Biology, University of Copenhagen, Copenhagen, Denmark. bregenberg@bio.ku.dk.ORCID http://orcid.org/0000-0003-4996-7012

Funding

Novo Nordisk NNF18OC0053139; NNF21OC0072023
6 · The paper itself

Abstract

eccDNA is a driver of many cancers and a potential intermediate in other age-related disorders. However, little is known about the mechanisms underlying eccDNA formation in healthy tissue and how aging affects these processes. Here, we present an atlas of eccDNA across seven tissues of male mice spanning four ages. EccDNA correlates with open chromatin characterized by signatures of H3K27ac and H3K4me1. Additionally, the mutational load of eccDNA on genes correlates with tissue-specific transcription and increases logarithmically as a function of transcript level. Still, a population of intron-dense genes with many splice forms remains sheltered from eccDNA formation. We also find that the total number of eccDNA molecules does not increase as mice age, unlike other types of mutations. Our data reveal a link between eccDNA formation and transcript level that may drive gene architecture in mammals.

Indexed as

DNATranscription, GeneticAgingAnimalsChromatinHistonesMaleMiceMutationChromatinDNAHistones

Identifiers

PMID39984484
PMCPMC11845583

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Registered trials

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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.