Evidence map›Paper›PMID 32328633›Full record

ArticleThe Journal of cell biology2020

Chromosomes function as a barrier to mitotic spindle bipolarity in polyploid cells.

Alix Goupil, Maddalena Nano, Gaëlle Letort, Simon Gemble, Frances Edwards, Oumou Goundiam, Delphine Gogendeau, Carole Pennetier, Renata Basto

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 39 citations in OpenAlex.

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  12. Ran GTPase and Its Importance in Cellular Signaling and Malignant Phenotype.International journal of molecular sciences · 2023
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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 at 2 institutions in 1 country.

Alix GoupilInstitut Curie, Paris Science et Lettres Research University, Centre National de la Recherche Scientifique, Unité Mixte de Recherche UMR144, Biology of Centrosomes and Genetic Instability Laboratory, Paris, France.
Maddalena NanoInstitut Curie, Paris Science et Lettres Research University, Centre National de la Recherche Scientifique, Unité Mixte de Recherche UMR144, Biology of Centrosomes and Genetic Instability Laboratory, Paris, France.
Gaëlle LetortCenter for Interdisciplinary Research in Biology, Collège de France, UMR7241/U1050, Paris, France.
Simon GembleInstitut Curie, Paris Science et Lettres Research University, Centre National de la Recherche Scientifique, Unité Mixte de Recherche UMR144, Biology of Centrosomes and Genetic Instability Laboratory, Paris, France.
Frances EdwardsInstitut Curie, Paris Science et Lettres Research University, Centre National de la Recherche Scientifique, Unité Mixte de Recherche UMR144, Biology of Centrosomes and Genetic Instability Laboratory, Paris, France.
Oumou GoundiamInstitut Curie, Paris Science et Lettres Research University, Centre National de la Recherche Scientifique, Unité Mixte de Recherche UMR144, Biology of Centrosomes and Genetic Instability Laboratory, Paris, France.
Delphine GogendeauInstitut Curie, Paris Science et Lettres Research University, Centre National de la Recherche Scientifique, Unité Mixte de Recherche UMR144, Biology of Centrosomes and Genetic Instability Laboratory, Paris, France.
Carole PennetierInstitut Curie, Paris Science et Lettres Research University, Centre National de la Recherche Scientifique, Unité Mixte de Recherche UMR144, Biology of Centrosomes and Genetic Instability Laboratory, Paris, France.
Renata BastoInstitut Curie, Paris Science et Lettres Research University, Centre National de la Recherche Scientifique, Unité Mixte de Recherche UMR144, Biology of Centrosomes and Genetic Instability Laboratory, Paris, France.
Centre National de la Recherche Scientifique · FRCollège de France · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ploidy variations such as genome doubling are frequent in human tumors and have been associated with genetic instability favoring tumor progression. How polyploid cells deal with increased centrosome numbers and DNA content remains unknown. Using Drosophila neuroblasts and human cancer cells to study mitotic spindle assembly in polyploid cells, we found that most polyploid cells divide in a multipolar manner. We show that even if an initial centrosome clustering step can occur at mitotic entry, the establishment of kinetochore-microtubule attachments leads to spatial chromosome configurations, whereby the final coalescence of supernumerary poles into a bipolar array is inhibited. Using in silico approaches and various spindle and DNA perturbations, we show that chromosomes act as a physical barrier blocking spindle pole coalescence and bipolarity. Importantly, microtubule stabilization suppressed multipolarity by improving both centrosome clustering and pole coalescence. This work identifies inhibitors of bipolar division in polyploid cells and provides a rationale to understand chromosome instability typical of polyploid cancer cells.

Indexed as

PolyploidyAnimalsCells, CulturedCentrosomeDrosophilaFemaleHEK293 CellsHumansSpindle Apparatus

Identifiers

PMID32328633
PMCPMC7147111
OpenAlexW3010256005

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.