Evidence map›Paper›PMID 26255654›Full record

ReviewChromosoma2016

How oocytes try to get it right: spindle checkpoint control in meiosis.

Sandra A Touati, Katja Wassmann

Abstract readReview
PubMed Publisher
In one paragraph

Review in Chromosoma, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 82 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Decoding Cdk1 control: from mitotic thresholds to meiotic specificity.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2026
    Review
  6. Article
  7. Article
  8. The Hallmarks of Aneuploidy in Cancer and Congenital Syndromes.Annual review of genomics and human genetics · 2025
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Double-checking chromosome segregation.The Journal of cell biology · 2023
    Review
  16. Genetic control of meiosis surveillance mechanisms in mammals.Frontiers in cell and developmental biology · 2023
    Review
  17. Prdm9 deficiency of rat oocytes causes synapsis among non-homologous chromosomes and aneuploidy.Mammalian genome : official journal of the International Mammalian Genome Society · 2022
    Article
  18. Article
  19. The process of ovarian aging: it is not just about oocytes and granulosa cells.Journal of assisted reproduction and genetics · 2022
    Review
  20. 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

2 authors at 1 institution in 2 countries.

Sandra A TouatiInstitut de Biologie Paris Seine (IBPS), UMR7622, Sorbonne Universités, UPMC Univ Paris 06, Paris, France.
Katja WassmannInstitut de Biologie Paris Seine (IBPS), UMR7622, Sorbonne Universités, UPMC Univ Paris 06, Paris, France. katja.wassmann@upmc.fr.
Sorbonne Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The generation of a viable, diploid organism depends on the formation of haploid gametes, oocytes, and spermatocytes, with the correct number of chromosomes. Halving the genome requires the execution of two consecutive specialized cell divisions named meiosis I and II. Unfortunately, and in contrast to male meiosis, chromosome segregation in oocytes is error prone, with human oocytes being extraordinarily "meiotically challenged". Aneuploid oocytes, that are with the wrong number of chromosomes, give rise to aneuploid embryos when fertilized. In humans, most aneuploidies are lethal and result in spontaneous abortions. However, some trisomies survive to birth or even adulthood, such as the well-known trisomy 21, which gives rise to Down syndrome (Nagaoka et al. in Nat Rev Genet 13:493-504, 2012). A staggering 20-25 % of oocytes ready to be fertilized are aneuploid in humans. If this were not bad enough, there is an additional increase in meiotic missegregations as women get closer to menopause. A woman above 40 has a risk of more than 30 % of getting pregnant with a trisomic child. Worse still, in industrialized western societies, child birth is delayed, with women getting their first child later in life than ever. This trend has led to an increase of trisomic pregnancies by 70 % in the last 30 years (Nagaoka et al. in Nat Rev Genet 13:493-504, 2012; Schmidt et al. in Hum Reprod Update 18:29-43, 2012). To understand why errors occur so frequently during the meiotic divisions in oocytes, we review here the molecular mechanisms at works to control chromosome segregation during meiosis. An important mitotic control mechanism, namely the spindle assembly checkpoint or SAC, has been adapted to the special requirements of the meiotic divisions, and this review will focus on our current knowledge of SAC control in mammalian oocytes. Knowledge on how chromosome segregation is controlled in mammalian oocytes may help to identify risk factors important for questions related to human reproductive health.

Indexed as

Cell Cycle CheckpointsMeiosisAneuploidyAnimalsChromosome SegregationFemaleHumansMaleOocytesSpindle ApparatusAneuploidyCohesin protectionMeiosisMonopolar attachmentMouse oocytesSpindle assembly checkpoint

Identifiers

PMID26255654
OpenAlexW1148878366

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.