Related Experiment Video For BUBR1
Updated: May 31, 2025

Evaluation of the Spindle Assembly Checkpoint Integrity in Mouse Oocytes
Published on: September 13, 2022
Sod1 deficiency in mouse oocytes during in vitro maturation increases chromosome segregation errors with a reduced
Mitsuru Nago1,2, Masumi Yanai1, Mika Ishii1
1Laboratory of Animal Reproduction, Graduate School of Agricultural Sciences Yamagata University Tsuruoka Japan.
Purpose:
This study aimed to investigate the molecular mechanisms associated with chromosome segregation errors caused by intrinsic oxidative stress during in vitro oocyte maturation (IVM) using oocytes from Sod1-deficient (Sod1KO) mice.
Methods:
Ovulated or in vitro matured cumulus-cells oocyte complexes (COCs) were collected from wild-type (WT) and Sod1KO mice and evaluated chromosome alignment, chromosome segregation, meiotic progression, and BUBR1 and REC8 protein expression levels.
Results:
In 21% O2 IVM, the Sod1KO had significantly higher frequencies of chromosome misalignment and segregation errors compared to the WT, and they also reached Germinal Vesicle Break Down (GVBD) and M I stages peak earlier and showed a shorter M I stage residence time compared to the WT. These changes were associated with a decrease in the recruitment of BUBR1 to kinetochores at M I stage, but there were no differences in the expression of REC8 between the two genotypes. Furthermore, the addition of L-ascorbic acid (AsA) or N-acetyl-L-cysteine (NAC) during IVM reduced the frequency of chromosome segregation errors in Sod1KO oocytes.
Conclusions:
Oxidative stress caused by Sod1 deficiency during IVM impairs the spindle assembly checkpoint function due to a decrease in the recruitment of BUBR1 to M I stage kinetochores, leading to abnormalities in meiotic progression and chromosome segregation.
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