Sexual differentiation in humans development can only occur when the fetal testis secretes key hormones at a critical period in early gestation. The testes begin to secrete three hormones that influence the male internal and external genitalia: they secrete anti-müllerian hormone (AMH), testosterone, and dihydrotestosterone (DHT). Anti-müllerian hormone causes the paramesonephric ducts to regress. Testosterone converts the mesonephric ducts into male accessory structures, including the epididymis, vas deferens, and seminal vesicle. Testosterone will also control the descending of the testes from the abdomen into the scrotum. Many other genes found on other autosomes, including"WT-1", "SOX9", "SF-1" also play a role in gonadal development. Females:
XX male syndrome gene on the Y chromosome is moved to become part of an X chromosome. The presence of the translocated SRY gene leads to an XX embryo developing male characteristics. In rare cases, an XX male does not have the SRY gene. The exact cause of this condition is unknown but it has been proposed that mutations in the SOX9 gene may contribute to this syndrome since SOX9 plays a role in testes differentiation during development. Another proposed cause is mutations to the DAX1 gene which encodes a nuclear hormone receptor. DAX1 represses masculinizing genes, therefore, if there is a loss