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Vol. 16, No. 11, pp. 1433-1440, June 1, 2002
1 Department of Cell Biology, Duke University Medical
Center, Durham, North Carolina 27710, USA; 2 Curis, Inc.,
Cambridge, Massachusetts 02138, USA
Establishment of the steroid-producing Leydig cell lineage is an
event downstream of Sry that is critical for masculinization of
mammalian embryos. Neither the origin of fetal Leydig cell precursors
nor the signaling pathway that specifies the Leydig cell lineage is
known. Based on the sex-specific expression patterns of Desert
Hedgehog (Dhh) and its receptor Patched 1 (Ptch1) in XY gonads, we investigated the potential role of
DHH/PTCH1 signaling in the origin and specification of fetal Leydig
cells. Analysis of Dhh
/ XY gonads revealed that
differentiation of fetal Leydig cells was severely defective. Defects
in Leydig cell differentiation in Dhh/ XY gonads
did not result from failure of cell migration from the mesonephros,
thought to be a possible source of Leydig cell precursors. Nor did
DHH/PTCH1 signaling appear to be involved in the proliferation or
survival of fetal Leydig precursors in the interstitium of the XY
gonad. Instead, our results suggest that DHH/PTCH1 signaling triggers
Leydig cell differentiation by up-regulating Steroidogenic Factor
1 and P450 Side Chain Cleavage enzyme expression in
Ptch1-expressing precursor cells located outside testis cords.
[Key Words: Desert Hedgehog; Patched 1; Leydig; mesonephros; testis; organogenesis]
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