Maternal SMC2 is essential for embryonic development via participating chromosome condensation in mice

During the oocyte growth, maturation and zygote development, chromatin structure keeps changing to regulate different nuclear activities. Here, we reported the role of SMC2, a core component of condensin complex, in oocyte and embryo development. Oocyte-specific conditional knockout of SMC2 caused female infertility. In the absence of SMC2, oocyte meiotic maturation and ovulation occurred normally, but chromosome condensation showed defects and DNA damages were accumulated in oocytes. The pronuclei were abnormally organized and micronuclei were frequently observed in fertilized eggs, their activity was impaired, and embryo development was arrested at the one-cell stage, suggesting that maternal SMC2 is essential for embryonic development. Summary of maternal SMC2 functions during oocyte growth, maturation and zygote development. In oocytes, the SMC2-deleted oocytes have defects in NSN-SN transition in GV stage, and further chromosome condensation. After fertilization, Depletion of maternal SMC2 causes abnormal nuclear morphology, impaired pronuclear function and accumulated DNA damage, which prevented the development of embryos beyond the zygote stage.image

Automated summary

The role of SMC2, a core component of condensin complex, in oocyte and embryo development was investigated. Deletion of SMC2 in oocytes caused female infertility, abnormal chromosome condensation, DNA damage, and impaired pronuclear function in fertilized eggs, leading to arrested embryo development at the one-cell stage.