Abstract
BackgroundPten 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.ResultsWe 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.ConclusionOur 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 materialThe online version of this article (doi:10.1186/s13578-015-0034-x) contains supplementary material, which is available to authorized users.
Highlights
Pten plays a crucial role in the stem cell maintenance in a few organs
In the stimulated by retinoic acid gene 8 (Stra8)-enhanced green fluorescent protein (EGFP) transgenic mice, spermatogonial stem cells can be labeled by EGFP as characterized by transplantation assay [14]
The phosphatase and tensin homolog (PTEN) signaling regulated the expression of promyelocytic leukaemia zinc finger (PLZF) and undifferentiated embryonic cell transcription factor 1 (UTF1) in spermatogonial stem cells (SSCs) We further examined the expression of glial cell-derived neurotrophic factor (GDNF) family receptor alpha-1 (GFRα1), PLZF and UTF1 in Pten-deleted testes at day 7 or day 10 using Western blot analysis
Summary
Pten plays a crucial role in the stem cell maintenance in a few organs. Pten defect 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. The precise balance of self-renewal and differentiation of stem cells is critical for the maintenance and function of a tissue or organ throughout life-time. PTEN signaling is critical in governing the stem cell pool in the blood system and central neural. The loss of Pten in ovary via conditional knockout triggers premature of oocytes and ovary aging [8]. To understand the function of Pten in regulating SSC fate and fertility in male mouse, we generated conditional Pten knockout males using germ cell specific Cre strain, the Stra8-Cre mouse. Conditional Pten knockout leads to depletion of SSC pool and infertility with age
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