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First published online 16 October 2008
doi: 10.1242/dev.024786

Development 135, 3745-3753 (2008)
Published by The Company of Biologists 2008
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Notch signaling maintains Leydig progenitor cells in the mouse testis

Hao Tang1, Jennifer Brennan1, Jeannie Karl1, Yoshio Hamada2, Lori Raetzman3 and Blanche Capel1,*

1 The Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.
2 The Department of Cellular Sociology, National Institute for Basic Biology, Okazaki, Japan.
3 Molecular and Integrative Physiology, University of Illinois at Urbana Champaign, IL 61801, USA.

* Author for correspondence (e-mail: b.capel{at}cellbio.duke.edu)

Accepted 15 September 2008

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.

Key words: Notch, Stem cells, Leydig cell, Germ cell, Testis cord, Hes1, Mouse






© The Company of Biologists Ltd 2008