Affordable Access

Access to the full text

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

Authors
  • SHIMOI, Gaku1
  • TOMITA, Masaru1
  • KATAOKA, Marino1
  • KAMEYAMA, Yuichi1
  • 1 Laboratory of Animal Resources and Development, Department of Northern Biosphere Agriculture, Faculty of Bioindustry, Tokyo University of Agriculture, Hokkaido 099-2493, Japan
Type
Published Article
Journal
The Journal of Reproduction and Development
Publisher
The Society for Reproduction and Development
Publication Date
Nov 22, 2018
Volume
65
Issue
1
Pages
57–66
Identifiers
DOI: 10.1262/jrd.2018-056
PMID: 30464155
PMCID: PMC6379765
Source
PubMed Central
Keywords
License
Green

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.

Report this publication

Statistics

Seen <100 times