Evidence map›Paper›PMID 31895940›Full record

ArticlePLoS biology2020

ATRX affects the repair of telomeric DSBs by promoting cohesion and a DAXX-dependent activity.

Courtney A Lovejoy, Kaori Takai, Michael S Huh, David J Picketts, Titia de Lange

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. ATRX safeguards cellular identity duringbioRxiv : the preprint server for biology · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Loss of function ofiScience · 2025
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Mutant ATRX: pathogenesis of ATRX syndrome and cancer.Frontiers in molecular biosciences · 2024
    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

5 authors at 3 institutions in 2 countries.

Courtney A LovejoyLaboratory for Cell Biology and Genetics, The Rockefeller University, New York, New York, United States of America.
Kaori TakaiLaboratory for Cell Biology and Genetics, The Rockefeller University, New York, New York, United States of America.ORCID 0000-0002-2631-8389
Michael S HuhRegenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.
David J PickettsRegenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.ORCID 0000-0002-9227-2016
Titia de LangeLaboratory for Cell Biology and Genetics, The Rockefeller University, New York, New York, United States of America.ORCID 0000-0002-9267-367X
Rockefeller University · USOttawa Hospital · CAUniversity of Ottawa · CA

Funding

MECHANISMS OF TELOMERE INDUCED SENESCENCER01AG016642 · NIA · ROCKEFELLER UNIVERSITY · PI Titia de Lange · 1999 to 2026
$11.9M
Genome instability in cancer: telomeres and DNA repairR35CA210036 · NCI · ROCKEFELLER UNIVERSITY · PI Titia de Lange · 2016 to 2026
$10.8M
TELOMERE LENGTH CONTROL BY TRF1 AND TRF2R01CA076027 · NCI · ROCKEFELLER UNIVERSITY · PI DE LANGE, TITIA · 1998 to 2012
$4.3M
CIHR MOP133586CIHR MOP142398NCI NIH HHS R01 CA076027NCI NIH HHS R35 CA210036NIA NIH HHS R01 AG016642
6 · The paper itself

Abstract

Alpha thalassemia/mental retardation syndrome X-linked chromatin remodeler (ATRX), a DAXX (death domain-associated protein) interacting protein, is often lost in cells using the alternative lengthening of telomeres (ALT) pathway, but it is not known how ATRX loss leads to ALT. We report that ATRX deletion from mouse cells altered the repair of telomeric double-strand breaks (DSBs) and induced ALT-like phenotypes, including ALT-associated promyelocytic leukemia (PML) bodies (APBs), telomere sister chromatid exchanges (T-SCEs), and extrachromosomal telomeric signals (ECTSs). Mechanistically, we show that ATRX affects telomeric DSB repair by promoting cohesion of sister telomeres and that loss of ATRX in ALT cells results in diminished telomere cohesion. In addition, we document a role for DAXX in the repair of telomeric DSBs. Removal of telomeric cohesion in combination with DAXX deficiency recapitulates all telomeric DSB repair phenotypes associated with ATRX loss. The data reveal that ATRX has an effect on telomeric DSB repair and that this role involves both telomere cohesion and a DAXX-dependent pathway.

Indexed as

DNA Breaks, Double-Strandedalpha-ThalassemiaAnimalsCells, CulturedCo-Repressor ProteinsDNA RepairEmbryo, MammalianFemaleHeLa CellsHumansMaleMiceMice, KnockoutMolecular ChaperonesSignal TransductionSister Chromatid ExchangeCo-Repressor ProteinsDAXX protein, humanDaxx protein, mouseMolecular ChaperonesX-linked Nuclear Protein

Identifiers

PMID31895940
PMCPMC6959610
OpenAlexW2997707658

What OpenQuestion holds

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LicenceCC BY
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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.