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.