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PTEN signaling is required for the maintenance of spermatogonial stem cells in mouse, by regulating the expressions of PLZF and UTF1

BACKGROUND: Pten plays a crucial role in the stem cell maintenance in a few organs. Pten defect also causes the premature oocytes and ovary aging. We and other groups have found that the phosphatidylinositol-3-OH kinase (PI3K)-Akt signaling regulates the proliferation and differentiation of spermato...

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Detalles Bibliográficos
Autores principales: Zhou, Wei, Shao, Hongfang, Zhang, Di, Dong, Jian, Cheng, Wei, Wang, Lu, Teng, Yincheng, Yu, Zhuo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4517568/
https://www.ncbi.nlm.nih.gov/pubmed/26221533
http://dx.doi.org/10.1186/s13578-015-0034-x
Descripción
Sumario:BACKGROUND: Pten plays a crucial role in the stem cell maintenance in a few organs. Pten defect also causes the premature oocytes and ovary aging. We and other groups have found that the phosphatidylinositol-3-OH kinase (PI3K)-Akt signaling regulates the proliferation and differentiation of spermatogonial stem cells (SSCs). PTEN functions as a negative regulator of the PI3K pathway. Thus, we thought that the fate of SSCs might be controlled by Pten. RESULTS: We report that promyelocytic leukaemia zinc finger (PLZF) and undifferentiated embryonic cell transcription factor 1 (UTF1), both of which are germ cell-specific transcriptional factors, are regulated by Pten. Conditional deletion of Pten leads to reduction in PLZF expression but induction of UTF1, which is associated with SSCs depletion and infertility in males with age. CONCLUSION: Our data demonstrate that Pten is required for the long-term maintenance of SSCs and precise regulation of spermatogenesis in mouse. The finding of a Pten-regulated GFRα1(+)/PLZF(−)/UTF1(+) progenitor population provides a new insight into the precise mechanisms controlling SSC fate. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13578-015-0034-x) contains supplementary material, which is available to authorized users.