Notch signaling maintains Leydig progenitor cells in the mouse testis.
Journal Article (Journal Article)
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.
Full Text
Duke Authors
Cited Authors
- Tang, H; Brennan, J; Karl, J; Hamada, Y; Raetzman, L; Capel, B
Published Date
- November 2008
Published In
Volume / Issue
- 135 / 22
Start / End Page
- 3745 - 3753
PubMed ID
- 18927153
Pubmed Central ID
- PMC3653410
International Standard Serial Number (ISSN)
- 0950-1991
Digital Object Identifier (DOI)
- 10.1242/dev.024786
Language
- eng
Conference Location
- England