Evidence map›Paper›PMID 24476913›Full record

ArticleNucleic acids research2014

The α isoform of topoisomerase II is required for hypercompaction of mitotic chromosomes in human cells.

Christine J Farr, Melissa Antoniou-Kourounioti, Michael L Mimmack, Arsen Volkov, Andrew C G Porter

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

37 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Cell confinement initiates a delayed but heritable loss of chromosomes.bioRxiv : the preprint server for biology · 2026
    Article
  3. Review
  4. Mitotic genome folding.The Journal of cell biology · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. BiallelicScience advances · 2022
    Article
  14. Article
  15. Mitotic chromosomes.Seminars in cell & developmental biology · 2021
    Review
  16. Article
  17. DNA topoisomerases: Advances in understanding of cellular roles and multi-protein complexes via structure-function analysis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2021
    Review
  18. Decoupling Growth and Protein Production in CHO Cells: A Targeted Approach.Frontiers in bioengineering and biotechnology · 2021
    Article
  19. DNA topoisomerases as molecular targets for anticancer drugs.Journal of enzyme inhibition and medicinal chemistry · 2020
    Review
  20. Topoisomerase IIα is essential for maintenance of mitotic chromosome structure.Proceedings of the National Academy of Sciences of the United States of America · 2020
    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 1 institution in 1 country.

Christine J FarrDepartment of Genetics, University of Cambridge, Downing St, Cambridge CB2 3EH, UK and Centre for Haematology, Faculty of Medicine, Imperial College London, Hammersmith Hospital Campus, Du Cane Rd, London W12 0NN, UK.
Melissa Antoniou-Kourounioti
Michael L Mimmack
Arsen Volkov
Andrew C G Porter
Hammersmith Hospital · GB

Funding

Cancer Research UK C9609/A10506Medical Research Council MRC DTG 2011
6 · The paper itself

Abstract

As proliferating cells transit from interphase into M-phase, chromatin undergoes extensive reorganization, and topoisomerase (topo) IIα, the major isoform of this enzyme present in cycling vertebrate cells, plays a key role in this process. In this study, a human cell line conditional null mutant for topo IIα and a derivative expressing an auxin-inducible degron (AID)-tagged version of the protein have been used to distinguish real mitotic chromosome functions of topo IIα from its more general role in DNA metabolism and to investigate whether topo IIβ makes any contribution to mitotic chromosome formation. We show that topo IIβ does contribute, with endogenous levels being sufficient for the initial stages of axial shortening. However, a significant effect of topo IIα depletion, seen with or without the co-depletion of topo IIβ, is the failure of chromosomes to hypercompact when delayed in M-phase. This requires much higher levels of topo II protein and is impaired by drugs or mutations that affect enzyme activity. A prolonged delay at the G2/M border results in hyperefficient axial shortening, a process that is topo IIα-dependent. Rapid depletion of topo IIα has allowed us to show that its function during late G2 and M-phase is truly required for shaping mitotic chromosomes.

Indexed as

Chromosomes, HumanAntigens, NeoplasmCatalytic DomainCell LineDNA-Binding ProteinsDNA Topoisomerases, Type IIG2 PhaseHumansMitosisMutationProtein IsoformsQuinolinesThiazolesAntigens, NeoplasmDNA-Binding ProteinsDNA Topoisomerases, Type IIProtein IsoformsQuinolinesRO 3306Thiazoles

Identifiers

PMID24476913
PMCPMC3985649
OpenAlexW2167415865

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.