Androgen receptor the development and maintenance of the male sexual phenotype. In some cell types, testosterone interacts directly with androgen receptors, whereas, in others, testosterone is converted by 5-alpha-reductase to dihydrotestosterone, an even more potent agonist for androgen receptor activation. Testosterone appears to be the primary androgen receptor-activating hormone in the Wolffian duct, whereas dihydrotestosterone is the main androgenic hormone in the urogenital sinus, urogenital tubercle, and hair follicles. Hence, testosterone is responsible primarily for the development of male primary sexual characteristics, whereas dihydrotestosterone is responsible for secondary male characteristics. Androgens cause slow epiphysis, or maturation of the bones, but more of
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