Research Paper Volume 10, Issue 2 pp 197—211
The role of autophagy during murine primordial follicle assembly
- 1 College of Animal Science and Technology, Northwest A&F University, Shaanxi Key Laboratory of Molecular Biology for Agriculture, Yangling Shaanxi, China
- 2 Institute of Reproductive Sciences, College of Life Sciences, Qingdao Agricultural University, Qingdao, China
- 3 Department of Reproductive Medicine, Qingdao Municipal Hospital, School of Medicine, Qingdao University, Qingdao, China
received: December 27, 2017 ; accepted: January 30, 2018 ; published: February 5, 2018 ;https://doi.org/10.18632/aging.101376
How to Cite
Copyright: Sun 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 is generally accepted that significant germ cell loss occurs during the establishment of the primordial follicle pool in most mammalian ovaries around the time of birth. However, the underlying mechanisms responsible for these processes remain largely unknown. In this investigation, we explored the role of autophagy during the establishment of the primordial follicle pool and found that autophagy was active in this process. Our data suggested that 17.5 dpc ovaries treated with rapamycin displayed a delay in germ cell cyst breakdown resulting in more oocytes at day 5 of treatment, while, ovaries that treated with 3-MA showed the opposite effect. We found that rapamycin treatment promoted autophagy and depressed cell apoptosis increasing the number of NOBOX positive oocytes. Furthermore, our results also revealed that epigenetic regulator, Sirt1, plays a role in germ cell loss. An epigenetic inhibitor or RNAi treatment of Sirt1, showed an increased level of H4K16ac and a decreased level of autophagy. Thus, these data indicate that autophagy prevents germ cell over loss during the establishment of primordial follicle pool, and this process may be influenced by Sirt1-invovled epigenetic regulation.
MVH: mouse vasa homolog; NOBOX: newborn ovary homeobox protein; LC3: microtubule-associated protein 1 light chain 3; TUNEL: TdT-mediated dUTP nick end labeling; dpp: days post partum; dpc: days post coitum; TEM: Transmission Electron Microscopy.