when the testis does not produce anti-müllerian hormone the müllerian ducts develop into
Anti-Müllerian hormone AMH is activated by SOX9 in the Sertoli cells of the male fetus.[4] Its expression inhibits the development of the female reproductive tract, or Müllerian ducts (paramesonephric ducts), in the male embryo, thereby arresting the development of fallopian tubes, uterus, and upper vagina.[5][6][7][8] AMH expression is critical to sex differentiation at a specific time during fetal development, and appears to be tightly regulated by nuclear receptor SF-1, transcription GATA factors, sex-reversal gene DAX1, and follicle-stimulating hormone (FSH).[9][10][11] Mutations in both the AMH gene and the type II AMH receptor have been shown to cause the persistence of Müllerian derivatives in males that are otherwise normally masculinized.[12]
Hypothalamic–pituitary–gonadal axis In males, the production of GnRH, LH, and FSH are similar, but the effects of these hormones are different.[8] FSH stimulates sustentacular cells to release androgen-binding protein, which promotes testosterone binding. LH binds to the interstitial cells, causing them to secrete testosterone. Testosterone is required for normal spermatogenesis and inhibits the hypothalamus. Inhibin is produced by the spermatogenic cells, which, also through inactivating activin, inhibits the hypothalamus. After puberty these hormones levels remain relatively constant.