Biol Reprod Keystone Symposia Conference on Frontiers in Reproductive Biology & Regulation of Fertility.
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BOR - Papers in Press, published online ahead of print January 8, 2003.
Biol Reprod 2003, 10.1095/biolreprod.102.012617
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BIOLOGY OF REPRODUCTION 68, 2033–2037 (2003)
DOI: 10.1095/biolreprod.102.012617
© 2003 by the Society for the Study of Reproduction, Inc.

Testis

Chemotactic Role of Neurotropin 3 in the Embryonic Testis That Facilitates Male Sex Determination1

Andrea S. Cupp3, Mehmet Uzumcu, and Michael K. Skinner2

Center for Reproductive Biology, School of Molecular Biosciences, Washington State University, Pullman, Washington 99164-4231

The first morphological event after initiation of male sex determination is seminiferous cord formation in the embryonic testis. Cord formation requires migration of pre-peritubular myoid cells from the adjacent mesonephros. The embryonic Sertoli cells are the first testicular cells to differentiate and have been shown to express neurotropin-3 (NT3), which can act on high-affinity trkC receptors expressed on migrating mesonephros cells. NT3 expression is elevated in the embryonic testis during the time of seminiferous cord formation. A trkC receptor tyrophostin inhibitor, AG879, was found to inhibit seminiferous cord formation and mesonephros cell migration. Beads containing NT3 were found to directly promote mesonephros cell migration into the gonad. Beads containing other growth factors such as epidermal growth factor (EGF) did not influence cell migration. At male sex determination the SRY gene promotes testis development and the expression of downstream sex differentiation genes such as SOX-9. Inhibition of NT3 actions caused a reduction in the expression of SOX-9. Combined observations suggest that when male sex determination is initiated, the developing Sertoli cells express NT3 as a chemotactic agent for migrating mesonephros cells, which are essential to promote embryonic testis cord formation and influence downstream male sex differentiation.

1 This study was supported by a grant from the National Institutes of Health to M.K.S.

2 Correspondence: Michael K. Skinner, Center for Reproductive Biology, P.O. Box 644234, School of Molecular Biosciences, Washington State University, Pullman, WA 99164-4231. FAX: 509 335 2176; skinner{at}mail.wsu.edu

3 Current address: Department of Animal Science, University of Nebraska, Lincoln, NE, 68583-0908






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Copyright © 2003 by the Society for the Study of Reproduction.