Journal of Andrology
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Published-Ahead-of-Print October 29, 2009, DOI:10.2164/jandrol.109.008318
Journal of Andrology, Vol. 31, No. 1, January/February 2010
Copyright © American Society of Andrology
DOI: 10.2164/jandrol.109.008318

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Part 1 - Regulation of Testis Development

Fetal Leydig Cells: Progenitor Cell Maintenance and Differentiation

IVRAYM B. BARSOUM* AND HUMPHREY H.-C. YAO{dagger}

From the * Department of Cell and Developmental Biology and the {dagger} Department of Veterinary Biosciences, University of Illinois at Urbana-Champaign, Urbana-Champaign, Illinois.

Correspondence to: Dr Humphrey H.-C. Yao, Department of Veterinary Biosciences, 3806 VMBSB, 2001 South Lincoln Ave, University of Illinois, Urbana, IL 61802 (e-mail: hhyao{at}illinois.edu).



Abstract

In most eutherian mammals, sexually dimorphic masculinization is established by androgen-producing fetal Leydig cells in the embryonic testis. Fetal Leydig cells, which lack expression of the testis-determining gene SRY, arise after the appearance of SRY-expressing Sertoli cells. Therefore, the appearance and differentiation of fetal Leydig cells are probably regulated by factors derived from Sertoli cells. Results from mouse genetic models have revealed that maintenance and differentiation of fetal Leydig cell population depends upon a balance between differentiation-promoting and differentiation-suppressing mechanisms. Although paracrine signaling via Sertoli cell–derived Hedgehog ligands is necessary and sufficient for fetal Leydig cell formation, cell-cell interaction via Notch signaling and intracellular transcription factors such as POD1 are implicated as suppressors of fetal Leydig cell differentiation. This review provides a model that summarizes the recent findings in fetal Leydig cell development.

     Key words: Reproductive genetics, testis, Hedgehog, Notch, steroidogenic factor 1




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