of the prostatic urethra at the center of the seminal colliculus. AMH receptor-type II (AMHR-II), also known as Misr-II, causes AMH to act indirectly on mesenchymal cells surrounding the paramesonephric ducts rather than acting directly on the epithelium of the duct. This receptor activation induces the ducts to regress. The importance of mesenchyme-to-epithelial signaling is to maintain AMHR-II expression in the mesenchyme. In the absence of the Wnta7a within the duct epithelium as the ducts regress, ductal AMHR-II expression is lost, and residual paramesonephric ducts would be retained in males, throwing off the urogenital system. Cryptorchidism (undescended testis) or ectopic testis with inguinal hernias have been identified in human males due to AMH and AMHR-II gene mutations. Studies have revealed another AMH receptor group, AMH receptor-type I (AMHR-I), based on the AMH being a TgfB/Bmp family member. Studies have shown that ALK2, Alk3 (or Bmpr 1a) and Alk6 all serve as AMHR-I receptors. When these receptors are blocked or knocked out in mice within the paramesonephric duct mesenchyme, AMH-induced paramesonephric duct regression is lost. Function In females, the paramesonephric ducts give rise to the uterine tubes, uterus, and upper portion of the vagina, while the mesonephric ducts degenerate due to the absence of male androgens. In contrast, the paramesonephric ducts begin to proliferate and differentiate in a cranial-caudal progression to form the aforementioned structures. During this time, the single-layered paramesonephric duct epithelium differentiates into other structures, ranging from the ciliated columnar epithelium in the uterine tube to stratified squamous epithelium in the vagina. The paramesonephric ducts and the mesonephric ducts share a majority of the same mesenchyme due to Hox gene expression. The genes expressed play a critical role in mediating the regional characterization of structures found along the cranial-caudal axis of the female reproductive tract. Clinical significance Mutations in AMH Individuals that are 46, XY and have been tested positive for mutations in their AMH or AMH receptor genes have been known to exhibit features typical of that which are exhibited in persistent müllerian duct syndrome due to the fact that the paramesonephric ducts fail to regress. When this happens the individuals develop structures that are derived from the paramesonephric duct, and also structures that are derived from the mesonephric duct. A male that has persistent müllerian duct syndrome may have an upper vagina, uterus, and uterine tubes as well as ductus deferens along with male external genitalia. The