Aurora B prevents aneuploidy via MAD2 during the first mitotic cleavage in oxidatively damaged embryos
A high rate of chromosome aneuploidy is exhibited in in vitro fertilization (IVF) derived embryos. Our previous experiments suggested that reactive oxygen species (ROS) can activate Mad2, a key protein in the spindle assembly checkpoint (SAC) and delay the first mitotic, providing time to prevent the formation of embryonic aneuploidy. We aimed to determine whether mitotic kinase Aurora B was involved in the SAC function to prevent aneuploidy in IVF derived embryos.
Cell proliferation