Reduced ability to recover from spindle disruption and loss of kinetochore spindle assembly checkpoint proteins in oocytes from aged mice

摘要: Currently, maternal aging in women, based on mouse models, is thought to raise oocyte aneuploidy rates, because chromosome cohesion deteriorates during prophase arrest, and Sgo2, a protector of centromeric cohesion, lost. Here we show that the most common strain, C57Bl6/J, resistant aging, showing little increase or Sgo2 loss. Instead it demonstrates significant kinetochore-associated loss spindle assembly checkpoint protein Mad2 phosphorylated Aurora C, which involved microtubule–kinetochore error correction. Their affects fidelity bivalent segregation but only when organization impaired maturation. These findings have an impact clinically regarding handling human oocytes ex vivo assisted reproductive techniques suggest there genetic basis susceptibility.