Investigation into the cause of oocyte aneuploidy using antioxidant capasity deficient mice and application to advanced IVM methods

2014 Fiscal Year Final Research Report

• Project/Area Number: 24580405
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Applied animal science
• Research Institution: Yamagata University
• Principal Investigator: KIMURA Naoko 山形大学, 農学部, 教授 (70361277)
• Co-Investigator(Renkei-kenkyūsha): FUJII Junichi 山形大学, 大学院医学研究科, 教授 (00222258)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 減数分裂 / 卵母細胞 / 異数性 / 酸化ストレス / 体外成熟,IVM / 紡錘体形成チェックポイント / 発生障害 / 老化

Outline of Final Research Achievements

This study was conducted to investigate effects of intrinsic oxidative stress using antioxidant capasity deficient mice during in vitro maturation (IVM).
SOD1-deficient oocytes under 20% O2 IVM substantially increased chromosome misalignment and a withering spindle assembly compared with wild-type oocytes or in vivo oocytes. SOD1-deficient oocytes accelerated the timing of germinal vesicle break down and progression of anaphase I compared with wild-type oocytes. The percentage of aneuploidy was two times higher in SOD1-deficient oocytes than in wild-type oocytes under 20% O2 IVM while in vivo oocytes showed similar percentage regardless of genotype. BubR1 signals on kinetocore were apparently weaken in SOD1-deficient oocytes compared with wild-type oocytes. Our results suggest that intrinsic oxidative stress during oocytes meiotic maturation impairs spindle assembly, regular timing of meiosis progression and localization of BubR1, which would consequently lead to aneuploidy.

Free Research Field

生殖生物学、生殖・発生工学