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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
22
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pubmed:dateCreated |
2008-10-27
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pubmed:abstractText |
During testis development, fetal Leydig cells increase their population from a pool of progenitor cells rather than from proliferation of a differentiated cell population. However, the mechanism that regulates Leydig stem cell self-renewal and differentiation is unknown. Here, we show that blocking Notch signaling, by inhibiting gamma-secretase activity or deleting the downstream target gene Hairy/Enhancer-of-split 1, results in an increase in Leydig cells in the testis. By contrast, constitutively active Notch signaling in gonadal somatic progenitor cells causes a dramatic Leydig cell loss, associated with an increase in undifferentiated mesenchymal cells. These results indicate that active Notch signaling restricts fetal Leydig cell differentiation by promoting a progenitor cell fate. Germ cell loss and abnormal testis cord formation were observed in both gain- and loss-of-function gonads, suggesting that regulation of the Leydig/interstitial cell population is important for male germ cell survival and testis cord formation.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0950-1991
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
135
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3745-53
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pubmed:dateRevised |
2010-12-3
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pubmed:meshHeading |
pubmed-meshheading:18927153-Amyloid Precursor Protein Secretases,
pubmed-meshheading:18927153-Animals,
pubmed-meshheading:18927153-Basic Helix-Loop-Helix Transcription Factors,
pubmed-meshheading:18927153-Cell Differentiation,
pubmed-meshheading:18927153-Cell Proliferation,
pubmed-meshheading:18927153-Embryo, Mammalian,
pubmed-meshheading:18927153-Enzyme Inhibitors,
pubmed-meshheading:18927153-Gene Expression Regulation, Developmental,
pubmed-meshheading:18927153-Homeodomain Proteins,
pubmed-meshheading:18927153-Leydig Cells,
pubmed-meshheading:18927153-Male,
pubmed-meshheading:18927153-Mice,
pubmed-meshheading:18927153-Mice, Transgenic,
pubmed-meshheading:18927153-Receptors, Notch,
pubmed-meshheading:18927153-Signal Transduction,
pubmed-meshheading:18927153-Stem Cells
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pubmed:year |
2008
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pubmed:articleTitle |
Notch signaling maintains Leydig progenitor cells in the mouse testis.
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pubmed:affiliation |
The Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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