Rad9a is required for spermatogonia differentiation in mice
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Lin Huang1,2, Zhen-Bo Wang2, Shu-Tao Qi1, Xue-Shan Ma2, Qiu-Xia Liang2,3, Guo Lei2, Tie-Gang Meng2, Li-Feng Liang1, Ye-Xin Xian1, Yi Hou2, Xiao-Fang Sun1, Yong Zhao4, Wei-Hua Wang1,5, Qing-Yuan Sun2,3
1Key Laboratory of Major Obstetrics Diseases of Guangdong Province, Key Laboratory of Reproduction and Genetics of Guangdong Higher Education Institutes, The Third Hospital Affiliated to Guangzhou Medical University, Guangdong, China
2State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China
3University of the Chinese Academy of Sciences, Beijing, China
4State Key Laboratory of Biomembrane, Institute of Zoology, Chinese Academy of Sciences, Beijing, China
5Houston Fertility Institute/Houston Fertility Laboratory, Houston, Texas, USA
Qing-Yuan Sun, email: [email protected]
Wei-Hua Wang, email: [email protected]
Keywords: RAD9A, Vasa, spermatogenesis, Sertoli cells, differentiation
Received: June 16, 2016 Accepted: November 09, 2016 Published: November 16, 2016
Spermatogenesis in testes requires precise spermatogonia differentiation. Spermatocytes lacking the Rad9a gene are arrested in pachytene prophase, implying a possible role for RAD9A in spermatogonia differentiation. However, numerous RAD9A-positive pachytene spermatocytes are still observed in mouse testes following Rad9a excision using the Stra8-Cre system, and it is unclear whether Rad9a deletion in spermatogonia interrupts differentiation. Here, we generated a mouse model in which Rad9a was specifically deleted in spermatogonial stem cells (SSCs) using Cre recombinase expression driven by the germ cell-specific Vasa promoter. Adult Rad9a-null male mice were infertile as a result of completely blocked spermatogonia differentiation. No early spermatocytes were detected in mutant testicular cords of 9-day-old mice. Mutant spermatogonia were prone to apoptosis, although proliferation rates were unaffected. Rad9a deletion also resulted in malformation of seminiferous tubules, in which cells assembled irregularly into clusters, and malformation led to testicular cord disruption. Our findings suggest that Rad9a is indispensable for spermatogonia differentiation and testicular development in mice.
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