Abstract
Premature ovarian failure (POF) in women is characterized as menopause commencing before age 35. Although some cases of POF appear to be inherited, no experimental animal models of familial POF are available. Recently a mouse mutation has been identified that results in infertility due to a lack of primordial germ cells arising in early embryonic development. It was observed that shortly after puberty, females homozygous for this mutation entered reproductive senescence as defined by high levels of circulating gonadotropins, inability to respond either hormonally or functionally to superovulation, and a disrupted estrous cycle. Also, the ovaries completely lacked developing follicles and the endometrium was inactive. However, these mice had undergone complete sexual development as determined by age of vaginal opening, mammary gland histology, and sexual behavior. Thus, these animals closely mimic familial premature ovarian failure and may be useful models for study of the pathogenesis and treatment of this condition.