Notch signaling maintains Leydig progenitor cells in the mouse testis

Hao Tang, Jennifer Brennan, Jeannie Karl, Yoshio Hamada, Lori Raetzman, Blanche Capel

Research output: Contribution to journalArticlepeer-review


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 γ-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-offunction gonads, suggesting that regulation of the Leydig/interstitial cell population is important for male germ cell survival and testis cord formation.

Original languageEnglish (US)
Pages (from-to)3745-3753
Number of pages9
Issue number22
StatePublished - 2008


  • Germ cell
  • Hes1
  • Leydig cell
  • Mouse
  • Notch
  • Stem cells
  • Testis cord

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology


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