Bibliographic Details
| Title: |
RAD51 is essential for spermatogenesis and male fertility in mice |
| Authors: |
Junchao Qin, Tao Huang, Jing Wang, Limei Xu, Qianli Dang, Xiuhua Xu, Hongbin Liu, Zhaojian Liu, Changshun Shao, Xiyu Zhang |
| Source: |
Cell Death Discovery, Vol 8, Iss 1, Pp 1-9 (2022) |
| Publisher Information: |
Nature Publishing Group, 2022. |
| Publication Year: |
2022 |
| Collection: |
LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
LCC:Cytology |
| Subject Terms: |
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282, Cytology, QH573-671 |
| More Details: |
Abstract The recombinase RAD51 catalyzes the DNA strand exchange reaction in homologous recombination (HR) during both mitosis and meiosis. However, the physiological role of RAD51 during spermatogenesis remains unclear since RAD51 null mutation is embryonic lethal in mice. In this study, we generated a conditional knockout mouse model to study the role of RAD51 in spermatogenesis. Conditional disruption of RAD51 in germ cells by Vasa-Cre led to spermatogonial loss and Sertoli cell-only syndrome. Furthermore, tamoxifen-inducible RAD51 knockout by UBC-CreERT2 confirmed that RAD51 deletion led to early spermatogenic cells loss and apoptosis. Notably, inducible knockout of RAD51 in adult mice caused defects in meiosis, with accumulated meiotic double-strand breaks (DSBs), reduced numbers of pachytene spermatocytes and less crossover formation. Our study revealed an essential role for Rad51 in the maintenance of spermatogonia as well as meiotic progression in mice. |
| Document Type: |
article |
| File Description: |
electronic resource |
| Language: |
English |
| ISSN: |
2058-7716 |
| Relation: |
https://doaj.org/toc/2058-7716 |
| DOI: |
10.1038/s41420-022-00921-w |
| Access URL: |
https://doaj.org/article/2ab31572ea9e4b97a80b0ce2248bea53 |
| Accession Number: |
edsdoj.2ab31572ea9e4b97a80b0ce2248bea53 |
| Database: |
Directory of Open Access Journals |
