Aurora B prevents aneuploidy via MAD2 during the first mitotic cleavage in oxidatively damaged embryos

Objectives 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. Materials and Methods We analysed aneuploidy formation and repair during embryo pre‐implantation via 4ʹ,6‐diamidino‐2‐phenylindole (DAPI) staining and karyotype analysis. We assessed Aurora B activation by immunofluorescence and investigated the effect of Aurora B inhibition on embryo injury‐related variables, such as embryonic development, ROS levels, mitochondrial membrane potential and γH2AX‐positive expression. Results We observed the expression and phosphorylation of Thr232 in Aurora B in oxidative stress‐induced zygotes. Moreover, inhibition of Aurora B caused chromosome mis‐segregation, abnormal spindle structures, abnormal chromosome number and reduced expression of Mad2 in IVF embryos. Our results suggest that Aurora B causes mitotic arrest and participates in SAC via Mad2 and H3S10P, which is required for self‐correction of aneuploidies. Conclusions We demonstrate here that oxidative stress–induced DNA damage triggers Aurora B‐mediated activation of SAC, which prevents aneuploidy at the first mitotic cleavage in early mouse IVF embryos.