Evidence map›Paper›PMID 24758999›Full record

ArticleCell cycle (Georgetown, Tex.)2014

Reduced ability to recover from spindle disruption and loss of kinetochore spindle assembly checkpoint proteins in oocytes from aged mice.

Yan Yun, Janet E Holt, Simon I R Lane, Eileen A McLaughlin, Julie A Merriman, Keith T Jones

Abstract 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 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing 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

40 citing papers in PubMed.

  1. Review
  2. Declining ribosome function limits oocyte longevity.bioRxiv : the preprint server for biology · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. The Reproductive Lifespan of Ovarian Follicle.Reproductive sciences (Thousand Oaks, Calif.) · 2024
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Meiotic spindle assembly checkpoint and aneuploidy in males versus females.Cellular and molecular life sciences : CMLS · 2019
    Review
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

6 authors.

Yan YunSchool of Biomedical Sciences & Pharmacy; University of Newcastle; Callaghan, NSW, Australia.
Janet E HoltSchool of Biomedical Sciences & Pharmacy; University of Newcastle; Callaghan, NSW, Australia.
Simon I R LaneSchool of Biomedical Sciences & Pharmacy; University of Newcastle; Callaghan, NSW, Australia; Centre for Biological Sciences; Faculty of Natural and Environmental Sciences; University of Southampton; Southampton, UK.
Eileen A McLaughlinSchool of Environmental and Life Sciences; University of Newcastle; Callaghan, NSW, Australia.
Julie A MerrimanSchool of Biomedical Sciences & Pharmacy; University of Newcastle; Callaghan, NSW, Australia; Centre for Biological Sciences; Faculty of Natural and Environmental Sciences; University of Southampton; Southampton, UK.
Keith T JonesSchool of Biomedical Sciences & Pharmacy; University of Newcastle; Callaghan, NSW, Australia; Centre for Biological Sciences; Faculty of Natural and Environmental Sciences; University of Southampton; Southampton, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Currently, maternal aging in women, based on mouse models, is thought to raise oocyte aneuploidy rates, because chromosome cohesion deteriorates during prophase arrest, and Sgo2, a protector of centromeric cohesion, is lost. Here we show that the most common mouse strain, C57Bl6/J, is resistant to maternal aging, showing little increase in aneuploidy or Sgo2 loss. Instead it demonstrates significant kinetochore-associated loss in the spindle assembly checkpoint protein Mad2 and phosphorylated Aurora C, which is involved in microtubule-kinetochore error correction. Their loss affects the fidelity of bivalent segregation but only when spindle organization is impaired during oocyte maturation. These findings have an impact clinically regarding the handling of human oocytes ex vivo during assisted reproductive techniques and suggest there is a genetic basis to aneuploidy susceptibility.

Indexed as

AgingAneuploidyAnimalsAurora Kinase CCell Cycle ProteinsChromosome SegregationFemaleKinetochoresMad2 ProteinsMiceMice, Inbred C57BLM Phase Cell Cycle CheckpointsNocodazoleOocytesSpecies SpecificitySpindle ApparatusAurora Kinase CCell Cycle ProteinsMad2l1 protein, mouseMad2 ProteinsNocodazoleSGOL2 protein, mouseaginganeuploidycell cycleerror correctionmeiosisoocytespindle assembly checkpoint

Identifiers

PMID24758999
PMCPMC4111757

What OpenQuestion holds

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Registered trials

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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.