Research Paper Volume 11, Issue 7 pp 1965—1976
SIRT6 participates in the quality control of aged oocytes via modulating telomere function
- 1 State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, China
- 2 Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China
Received: January 2, 2019 Accepted: March 20, 2019 Published: March 29, 2019https://doi.org/10.18632/aging.101885
How to Cite
Copyright: Ge 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.
It has been well recognized that oocyte quality declines in aging animals. However, to date, the underlying mechanism remains to be explored. In the present study, we report that oocytes and embryos from aged mice (42-45 weeks old) display the reduced expression of SIRT6 protein, accompanying with telomere shortening and DNA lesions. Moreover, we demonstrate that specific depletion of SIRT6 in oocytes induces dysfunctional telomeres and apoptosis of the resultant early embryos, leading to the developmental delay and cytoplasmic fragmentation. Importantly, we further find that overexpression of SIRT6 in aged oocytes promotes the telomere elongation in 2-cell embryos and lowers the incidence of apoptotic blastomeres. In summary, our data indicate a role for SIRT6 in modulating telomere function during oocyte maturation and embryonic development, and discover that SIRT6 reduction is an important point connecting maternal aging and quality control of oocyte/embryos.