Hormonal regulation of male reproductive tract development

We have employed gene knockout technology in mice to probe gene function in various stages of mouse male sexual differentiation. Insulin-like factor (Ins13) is prominently expressed in Leydig cells. Mutation of this gene leads to fully penetrant cryptorchidism. Single mutation in each of the three known insulin family receptor tyrosine kinases alone has limited effects on sexual differentiation; however, compound mutations result in formation of ovotestes, and triple mutations cause male-to-female sexual reversal. The implications of our mouse models are discussed.