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BioMed Research International
Volume 2014 (2014), Article ID 154251, 11 pages
Research Article

miRNA Signature in Mouse Spermatogonial Stem Cells Revealed by High-Throughput Sequencing

1Yunnan Key Laboratory of Primate Biomedical Research, No. 1 Boda Road, Yuhua Area, Chenggong District, Kunming, Yunnan 650500, China
2State Key Laboratory of Genetic Resources and Evolution, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan 650223, China
3Kunming Biomed International and National Engineering Research Center of Biomedicine and Animal Science, Kunming, Yunnan 650500, China
4Department of Medicine, School of Medicine, Vanderbilt University, Nashville, TN 37203, USA

Received 21 May 2014; Accepted 20 June 2014; Published 17 July 2014

Academic Editor: Zhixiang Lu

Copyright © 2014 Tao Tan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Spermatogonial stem cells (SSCs) play fundamental roles in spermatogenesis. Although a handful of genes have been discovered as key regulators of SSC self-renewal and differentiation, the regulatory network responsible for SSC function remains unclear. In particular, small RNA signatures during mouse spermatogenesis are not yet systematically investigated. Here, using next generation sequencing, we compared small RNA signatures of in vitro expanded SSCs, testis-derived somatic cells (Sertoli cells), developing germ cells, mouse embryonic stem cells (ESCs), and mouse mesenchymal stem cells among mouse embryonic stem cells (ESCs) to address small RNA transition during mouse spermatogenesis. The results manifest that small RNA transition during mouse spermatogenesis displays overall declined expression profiles of miRNAs and endo-siRNAs, in parallel with elevated expression profiles of piRNAs, resulting in the normal biogenesis of sperms. Meanwhile, several novel miRNAs were preferentially expressed in mouse SSCs, and further investigation of their functional annotation will allow insights into the mechanisms involved in the regulation of SSC activities. We also demonstrated the similarity of miRNA signatures between SSCs and ESCs, thereby providing a new clue to understanding the molecular basis underlying the easy conversion of SSCs to ESCs.