Evidence map›Paper›PMID 30464155›Full record

ArticleThe Journal of reproduction and development2019

Destabilization of spindle assembly checkpoint causes aneuploidy during meiosis II in murine post-ovulatory aged oocytes.

Gaku Shimoi, Masaru Tomita, Marino Kataoka, Yuichi Kameyama

Open access · goldAbstract read
In one paragraph

Article in The Journal of reproduction and development, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

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  15. Molecular basis of reproductive senescence: insights from model organisms.Journal of assisted reproduction and genetics · 2021
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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

4 authors at 1 institution in 1 country.

Gaku ShimoiLaboratory of Animal Resources and Development, Department of Northern Biosphere Agriculture, Faculty of Bioindustry, Tokyo University of Agriculture, Hokkaido 099-2493, Japan.
Masaru TomitaLaboratory of Animal Resources and Development, Department of Northern Biosphere Agriculture, Faculty of Bioindustry, Tokyo University of Agriculture, Hokkaido 099-2493, Japan.
Marino KataokaLaboratory of Animal Resources and Development, Department of Northern Biosphere Agriculture, Faculty of Bioindustry, Tokyo University of Agriculture, Hokkaido 099-2493, Japan.
Yuichi KameyamaLaboratory of Animal Resources and Development, Department of Northern Biosphere Agriculture, Faculty of Bioindustry, Tokyo University of Agriculture, Hokkaido 099-2493, Japan.
Tokyo University of Agriculture · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mammalian oocyte quality degrades over time after ovulation in vitro, which can cause fatal defects such as chromosomal aneuploidy. As various oocyte manipulations employed in assisted reproductive technology are time consuming, post-ovulatory aging is a serious problem to overcome in reproductive medicine or ova research. In this study, we investigated the effects of postovulatory aging on the incidence of chromosome aneuploidy during meiosis II, with a focus on the expression of functional proteins from the spindle assembly checkpoint (SAC). Chromosome analysis was used to assess the rate of aneuploidy in in vitro aged oocytes, or in early embryos derived from aged oocytes. Immunofluorescent staining was used to detect the localization of MAD2, which is a SAC signal that monitors the correct segregation of sister chromatids. Immunoblotting was used to quantify cohesin subunits, which are adhesion factors connecting sister chromatids at the metaphase II (MII) centromere. It was shown that post-ovulatory oocyte aging inhibits MAD2 localization to the sister kinetochore. Furthermore, oocyte aging prevented cohesin subunits from being maintained or degraded at the appropriate time. These data suggest that the destabilization of SAC signaling causes sister chromatid segregation errors in MII oocytes, and consequently increases the incidence of aneuploidy in early embryos. Our findings have provided distinct evidence that the post-ovulatory aging of oocytes might also be a risk factor for aneuploidy, irrespective of maternal age.

Indexed as

AneuploidyAnimalsCell Cycle ProteinsCellular SenescenceChromosomal Proteins, Non-HistoneCohesinsEmbryo, MammalianFemaleFertilization in VitroFluorescent Antibody TechniqueIn Vitro Oocyte Maturation TechniquesKinetochoresMad2 ProteinsMaleMeiosisMiceCell Cycle ProteinsChromosomal Proteins, Non-HistoneCohesinsMad2l1 protein, mouseMad2 ProteinsAneuploidyCohesinMAD2Postovulatory agingSpindle assembly checkpoint

Identifiers

PMID30464155
PMCPMC6379765
OpenAlexW2901361439

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.