Evidence map›Paper›PMID 31395887›Full record

ArticleNature communications2019

Mild replication stress causes chromosome mis-segregation via premature centriole disengagement.

Therese Wilhelm, Anna-Maria Olziersky, Daniela Harry, Filipe De Sousa, Helène Vassal, Anja Eskat, Patrick Meraldi

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

88 citing papers in PubMed, 136 citations in OpenAlex.

  1. Review
  2. Article
  3. Unraveling the Molecular Mechanisms Underlying Spontaneous Multipolar Mitosis Through CIN-seq.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  9. CHAMP1 complex promotes heterochromatin assembly and reduces replication stress.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  11. Article
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  17. Review
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  19. Targeting chromosomal instability in patients with cancer.Nature reviews. Clinical oncology · 2024
    Review
  20. Article

28 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 2 countries.

Therese WilhelmDepartment of Cell Physiology and Metabolism, University of Geneva, 1211, Geneva 4, Switzerland. Therese.Wilhelm@gustaveroussy.fr.
Anna-Maria OlzierskyDepartment of Cell Physiology and Metabolism, University of Geneva, 1211, Geneva 4, Switzerland.
Daniela HarryDepartment of Cell Physiology and Metabolism, University of Geneva, 1211, Geneva 4, Switzerland.
Filipe De SousaDepartment of Cell Physiology and Metabolism, University of Geneva, 1211, Geneva 4, Switzerland.
Helène VassalDepartment of Cell Physiology and Metabolism, University of Geneva, 1211, Geneva 4, Switzerland.
Anja EskatDepartment of Cell Physiology and Metabolism, University of Geneva, 1211, Geneva 4, Switzerland.
Patrick MeraldiDepartment of Cell Physiology and Metabolism, University of Geneva, 1211, Geneva 4, Switzerland. Patrick.Meraldi@unige.ch.
University of Geneva · CHInstitute of Nuclear Physics of Lyon · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Replication stress, a hallmark of cancerous and pre-cancerous lesions, is linked to structural chromosomal aberrations. Recent studies demonstrated that it could also lead to numerical chromosomal instability (CIN). The mechanism, however, remains elusive. Here, we show that inducing replication stress in non-cancerous cells stabilizes spindle microtubules and favours premature centriole disengagement, causing transient multipolar spindles that lead to lagging chromosomes and micronuclei. Premature centriole disengagement depends on the G2 activity of the Cdk, Plk1 and ATR kinases, implying a DNA-damage induced deregulation of the centrosome cycle. Premature centriole disengagement also occurs spontaneously in some CIN+ cancer cell lines and can be suppressed by attenuating replication stress. Finally, we show that replication stress potentiates the effect of the chemotherapeutic agent taxol, by increasing the incidence of multipolar cell divisions. We postulate that replication stress in cancer cells induces numerical CIN via transient multipolar spindles caused by premature centriole disengagement.

Indexed as

Chromosomal InstabilityChromosome SegregationAntineoplastic Agents, PhytogenicCarcinogenesisCell Line, TumorCentriolesDNA DamageG2 Phase Cell Cycle CheckpointsHumansMicrotubulesNeoplasmsPaclitaxelSpindle ApparatusStress, PhysiologicalAntineoplastic Agents, PhytogenicPaclitaxel

Identifiers

PMID31395887
PMCPMC6687892
OpenAlexW2966553109

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.