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Research Paper|Volume 12, Issue 11|pp 10415—10426

CHK2 is essential for spindle assembly and DNA repair during the first cleavage of mouse embryos

Xiao-Han Li1, Wen-Jing Li2, Jia-Qian Ju1, Meng-Hao Pan1, Yao Xu1, Ming-Hong Sun1, Mo Li2, Shao-Chen Sun1
  • 1College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China
  • 2Center for Reproductive Medicine, Peking University Third Hospital, Beijing 100191, China
* Equal contribution
Received: February 11, 2020Accepted: April 20, 2020Published: June 2, 2020
https://doi.org/10.18632/aging.103267

Copyright © 2020 Li et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The quality of the early embryo is critical for embryonic development and implantation. Errors during cleavage lead to aneuploidy in embryos. As a cell cycle checkpoint protein, CHK2 participates in DNA replication, cell cycle arrest and spindle assembly. However, the functions of CHK2 in early development of the mouse embryo remain largely unknown. In this study, we show that CHK2 is localized on the spindle in metaphase and mainly accumulates at spindle poles in anaphase/telophase during the first cleavage of the mouse embryo. CHK2 inhibition led to cleavage failure in early embryonic development, accompanied by abnormal spindle assembly and misaligned chromosomes. Moreover, the loss of CHK2 activity increased the level of cellular DNA damage, which resulted in oxidative stress. Then, apoptosis and autophagy were found to be active in these embryos. In summary, our results suggest that CHK2 is an essential regulator of spindle assembly and DNA repair during early embryonic development in mice.