期刊
STEM CELLS
卷 34, 期 11, 页码 2772-2783出版社
WILEY-BLACKWELL
DOI: 10.1002/stem.2449
关键词
GLIS3; Spermatogonial stem cell; Spermatogenesis; Gene expression
资金
- Intramural Research Program of the National Institute of Environmental Health Sciences, National Institutes of Health [Z01-ES-100485]
In this study, we identify a novel and essential role for the Kruppel-like zinc finger transcription factor GLI-similar 3 (GLIS3) in the regulation of postnatal spermatogenesis. We show that GLIS3 is expressed in gonocytes, spermatogonial stem cells (SSCs) and spermatogonial progenitors (SPCs), but not in differentiated spermatogonia and later stages of spermatogenesis or in somatic cells. Spermatogenesis is greatly impaired in GLIS3 knockout mice. Loss of GLIS3 function causes a moderate reduction in the number of gonocytes, but greatly affects the generation of SSCs/SPCs, and as a consequence the development of spermatocytes. Gene expression profiling demonstrated that the expression of genes associated with undifferentiated spermatogonia was dramatically decreased in GLIS3-deficient mice and that the cytoplasmic-to-nuclear translocation of FOXO1, which marks the gonocyte-to-SSC transition and is necessary for SSC self-renewal, is inhibited. These observations suggest that GLIS3 promotes the gonocyte-to-SSC transition and is a critical regulator of the dynamics of early postnatal spermatogenesis.
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