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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...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2015
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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 |
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author | Zhou, Wei Shao, Hongfang Zhang, Di Dong, Jian Cheng, Wei Wang, Lu Teng, Yincheng Yu, Zhuo |
author_facet | Zhou, Wei Shao, Hongfang Zhang, Di Dong, Jian Cheng, Wei Wang, Lu Teng, Yincheng Yu, Zhuo |
author_sort | Zhou, Wei |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-4517568 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-45175682015-07-29 PTEN signaling is required for the maintenance of spermatogonial stem cells in mouse, by regulating the expressions of PLZF and UTF1 Zhou, Wei Shao, Hongfang Zhang, Di Dong, Jian Cheng, Wei Wang, Lu Teng, Yincheng Yu, Zhuo Cell Biosci Research 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. BioMed Central 2015-07-28 /pmc/articles/PMC4517568/ /pubmed/26221533 http://dx.doi.org/10.1186/s13578-015-0034-x Text en © Zhou et al. 2015 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Zhou, Wei Shao, Hongfang Zhang, Di Dong, Jian Cheng, Wei Wang, Lu Teng, Yincheng Yu, Zhuo PTEN signaling is required for the maintenance of spermatogonial stem cells in mouse, by regulating the expressions of PLZF and UTF1 |
title | PTEN signaling is required for the maintenance of spermatogonial stem cells in mouse, by regulating the expressions of PLZF and UTF1 |
title_full | PTEN signaling is required for the maintenance of spermatogonial stem cells in mouse, by regulating the expressions of PLZF and UTF1 |
title_fullStr | PTEN signaling is required for the maintenance of spermatogonial stem cells in mouse, by regulating the expressions of PLZF and UTF1 |
title_full_unstemmed | PTEN signaling is required for the maintenance of spermatogonial stem cells in mouse, by regulating the expressions of PLZF and UTF1 |
title_short | PTEN signaling is required for the maintenance of spermatogonial stem cells in mouse, by regulating the expressions of PLZF and UTF1 |
title_sort | pten signaling is required for the maintenance of spermatogonial stem cells in mouse, by regulating the expressions of plzf and utf1 |
topic | Research |
url | 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 |
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