Androgen supplementation partially rescued testicular descent but not hypospadias in Gli3 XtJ mutants, decoupling local effects of GLI3 loss from systemic effects of androgen insufficiency. Fetal Leydig cells, the sole source of these hormones in developing testis, were reduced in numbers in Gli3 XtJ testes, and their functional identity diminished over time.
We found that Gli3 XtJ mutant mice exhibit cryptorchidism and hypospadias due to local effects of GLI3 loss and systemic effects of testicular hormone deficiency. Male urogenital development requires Hedgehog-GLI signaling and testicular hormones, but how these pathways interact is unclear. Urogenital tract abnormalities are among the most common congenital defects in humans.
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