Age-related chromosomal aneuploidy in oocytes is one of the significant factors contributing to female infertility, miscarriage, and neonatal malformations. Currently, there are no preventive or therapeutic measures other than screening and induced abortion in clinical practice. SUMOylated modification regulates the meiotic process of oocytes, and abnormal SUMOylation leads to aneuploidy in oocytes. However, it is still unclear which targets modified by SUMOylation are key factors to affect oocyte aneuploidy, which numerous proteins are SUMOylated in oocytes. Therefore, it focuses on exploring the key targets of SUMOylation modification inducing oocyte aneuploidy in this study. The results shows that PLK1 and Aurora-A undergo SUMOylation mediated by SUMO-1 and SUMO-2/3 in oocytes, while SGO2 and Aurora-B only undergo SUMOylation mediated by SUMO-2/3. SUMOylated site mutants of key targets are employed to prevent the side-effects of inhibitor on all SUMOylated proteins. The results shows that SUMOylation directly modifies and controls the recruitment of key targets, including PLK1, Aurora-A, and Aurora-B, to modulate spindle formation. On the other hand, SUMOylation of SGO2 controls the recruitment of SGO2 on the chromosome arms rather than on centromere. It does not contribute in spindle formation, and might participate in the regulation of correct chromosome segregation through the kinetochore-heterochromatin pathway. It reveals the key target factors of SUMOylation modification to the induction of oocyte chromosomal aneuploidy, providing a theoretical basis for the clinical prevention and treatment of infertility, miscarriage, and neonatal birth defects caused by oocyte chromosomal aneuploidy in this study.

Oocytes, Meiosis, SUMOylation, Recruitment