| First Author | Tang H | Year | 2008 |
| Journal | Development | Volume | 135 |
| Issue | 22 | Pages | 3745-53 |
| PubMed ID | 18927153 | Mgi Jnum | J:143587 |
| Mgi Id | MGI:3828215 | Doi | 10.1242/dev.024786 |
| Citation | Tang H, et al. (2008) Notch signaling maintains Leydig progenitor cells in the mouse testis. Development 135(22):3745-53 |
| 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. |
