Evidence map›Paper›PMID 33073400›Full record

ArticleThe EMBO journal2020

Microtubule poleward flux in human cells is driven by the coordinated action of four kinesins.

Yulia Steblyanko, Girish Rajendraprasad, Mariana Osswald, Susana Eibes, Ariana Jacome, Stephan Geley, António J Pereira, Helder Maiato, Marin Barisic

Abstract read
In one paragraph

Article in The EMBO journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing 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

53 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Design principles for self-organization of mitotic spindle bipolarity.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Article
  13. Mechanism and regulation of kinesin motors.Nature reviews. Molecular cell biology · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. Microtubule poleward flux as a target for modifying chromosome segregation errors.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  18. Article
  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

9 authors.

Yulia SteblyankoDanish Cancer Society Research Center (DCRC), Copenhagen, Denmark.
Girish RajendraprasadDanish Cancer Society Research Center (DCRC), Copenhagen, Denmark.
Mariana Osswaldi3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.
Susana EibesDanish Cancer Society Research Center (DCRC), Copenhagen, Denmark.
Ariana Jacomei3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.
Stephan GeleyInstitute of Pathophysiology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.
António J Pereirai3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.
Helder Maiatoi3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.
Marin BarisicDanish Cancer Society Research Center (DCRC), Copenhagen, Denmark.ORCID 0000-0001-7587-3867

Funding

EC | H2020 | H2020 Priority Excellent Science | H2020 European Research Council (ERC) 681443Kraeftens Bekaempelse (DCS) R146-A9322Lundbeckfonden (Lundbeck Foundation) R215-2015-4081Novo Nordisk Fonden (NNF) NNF19OC0058504
6 · The paper itself

Abstract

Mitotic spindle microtubules (MTs) undergo continuous poleward flux, whose driving force and function in humans remain unclear. Here, we combined loss-of-function screenings with analysis of MT-dynamics in human cells to investigate the molecular mechanisms underlying MT-flux. We report that kinesin-7/CENP-E at kinetochores (KTs) is the predominant driver of MT-flux in early prometaphase, while kinesin-4/KIF4A on chromosome arms facilitates MT-flux during late prometaphase and metaphase. Both these activities work in coordination with kinesin-5/EG5 and kinesin-12/KIF15, and our data suggest that the MT-flux driving force is transmitted from non-KT-MTs to KT-MTs by the MT couplers HSET and NuMA. Additionally, we found that the MT-flux rate correlates with spindle length, and this correlation depends on the establishment of stable end-on KT-MT attachments. Strikingly, we find that MT-flux is required to regulate spindle length by counteracting kinesin 13/MCAK-dependent MT-depolymerization. Thus, our study unveils the long-sought mechanism of MT-flux in human cells as relying on the coordinated action of four kinesins to compensate for MT-depolymerization and regulate spindle length.

Indexed as

Cell Cycle ProteinsChromosomesHumansKinesinsMetaphaseMicrotubulesMitosisSpindle ApparatusCell Cycle ProteinsKIF15 protein, humanKinesinsNUMA1 protein, humankinesinskinetochoremicrotubulesmitosismitotic spindle

Identifiers

PMID33073400
PMCPMC7705458

What OpenQuestion holds

Textmetadata
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.