Evidence map›Paper›PMID 24626180›Full record

ArticleCell cycle (Georgetown, Tex.)2014

TopoIIα prevents telomere fragility and formation of ultra thin DNA bridges during mitosis through TRF1-dependent binding to telomeres.

Martina Stagno d'Alcontres, Jose Alejandro Palacios, Diego Mejias, Maria A Blasco

Open access · hybridAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2014. 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
1.7field-weighted citation impact, top 16% 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, 42 citations in OpenAlex.

  1. Article
  2. Review
  3. Telomere maintenance and the DNA damage response: a paradoxical alliance.Frontiers in cell and developmental biology · 2024
    Article
  4. Review
  5. Article
  6. Article
  7. Telomere Replication: Solving Multiple End Replication Problems.Frontiers in cell and developmental biology · 2021
    Review
  8. Article
  9. Review
  10. Review
  11. The many lives of type IA topoisomerases.The Journal of biological chemistry · 2020
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

4 authors at 2 institutions in 2 countries.

Martina Stagno d'AlcontresTelomeres and Telomerase Group; Molecular Oncology Programme; Spanish National Cancer Research Centre (CNIO); Madrid, Spain.
Jose Alejandro PalaciosTelomeres and Telomerase Group; Molecular Oncology Programme; Spanish National Cancer Research Centre (CNIO); Madrid, Spain.
Diego MejiasConfocal Microscopy Unit; Biotechnology Programme; Spanish National Cancer Research Centre (CNIO); Madrid, Spain.
Maria A BlascoTelomeres and Telomerase Group; Molecular Oncology Programme; Spanish National Cancer Research Centre (CNIO); Madrid, Spain.
Molecular Oncology (United States) · USSpanish National Cancer Research Centre · ES

Funding

European Research Council 232854
6 · The paper itself

Abstract

Telomeres are repetitive nucleoprotein structures at the ends of chromosomes. Like most genomic regions consisting of repetitive DNA, telomeres are fragile sites prone to replication fork stalling and generation of chromosomal instability. In particular, abrogation of the TRF1 telomere binding protein leads to stalled replication forks and aberrant telomere structures known as "multitelomeric signals". Here, we report that TRF1 deficiency also leads to the formation of "ultra-fine bridges" (UFB) during mitosis, and to an increased time to complete mitosis mediated by the spindle assembly checkpoint proteins (SAC). We find that topoisomerase IIα (TopoIIα), an enzyme essential for resolution of DNA replication intermediates, binds telomeres in a TRF1-mediated manner. Indeed, similar to TRF1 abrogation, TopoIIα downregulation leads to telomere fragility and UFB, suggesting that these phenotypes are due to decreased TopoIIα at telomeres. We find that SAC proteins bind telomeres in vivo, and that this is disrupted upon TRF1 deletion. These findings suggest that TRF1 links TopoIIα and SAC proteins in a pathway that ensures correct telomere replication and mitotic segregation, unveiling how TRF1 protects from telomere fragility and mitotic defects.

Indexed as

Chromosome Fragile SitesAntigens, NeoplasmCell Cycle ProteinsCell Line, TumorDNADNA-Binding ProteinsDNA Topoisomerases, Type IIHumansMicrotubule-Associated ProteinsMitosisM Phase Cell Cycle CheckpointsNuclear ProteinsProtein Serine-Threonine KinasesTelomereTelomeric Repeat Binding Protein 1Antigens, NeoplasmBUB1 protein, humanCell Cycle ProteinsDNADNA-Binding ProteinsDNA Topoisomerases, Type IIMAD1L1 protein, humanMicrotubule-Associated ProteinsNuclear ProteinsProtein Serine-Threonine KinasesTelomeric Repeat Binding Protein 1fragilitymitosisSACShelterinTopoIITRF1

Identifiers

PMID24626180
PMCPMC4050144
OpenAlexW2070043307

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.