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:
Growth-hormone-releasing hormone receptor to date. Growth-hormone-releasing hormone receptor The growth-hormone-releasing hormone receptor (GHRHR) is a G-protein-coupled receptor that binds growth hormone-releasing hormone. The GHRHR activates a Gs protein that causes a cascade of cAMP via Adenylate cyclase. This gene, expressed in the pituitary, encodes a receptor for growth-hormone-releasing hormone. Binding of this hormone to the receptor leads to synthesis and release of growth hormone. Mutations in this gene have been associated with isolated growth-hormone deficiency (IGHD), also known as Dwarfism of Sindh, a disorder characterized by short stature. Many alternate transcriptional splice variants encoding different isoforms have been described, but only two have