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Follicle stimulating hormone is required for ovarian follicle maturation but not male fertility

Abstract

Follicle stimulating hormone (FSH) is a member of the glycoprotein hormone family that includes luteinizing hormone (LH), thyroid stimulating hormone, and chorionic gonadotropin. These heterodimeric hormones share a common α subunit and differ in their hormone-specific β subunit. The biological activity is conferred only by the heterodimers. FSH and LH are synthesized in the same cells of the pituitary, the gonadotrophs1,2. FSH receptors are localized to Sertoli cells of the testes and granulosa cells of the ovary1,2. Minimal data has been accumulated so far involving human mutations in the FSHβ, LHβ, or the gonadotropin receptor genes. There are no known mouse strains with mutations in the FSHβ gene. To generate animal models for human diseases involving the gonadotropin signal transduction pathway, we produced mice deficient in the FSHβ subunit and therefore in FSH using ES cell technology. FSH-deficient females are infertile due to a block in folliculogenesis prior to antral follicle formation. Although FSH was predicted to be necessary for spermatogenesis and Sertoli cell growth in males, FSH-deficient males are fertile despite having small testes. Our findings have important implications for male contraceptive development in humans.

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Correspondence to Martin M. Matzuk.

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Kumar, T., Wang, Y., Lu, N. et al. Follicle stimulating hormone is required for ovarian follicle maturation but not male fertility. Nat Genet 15, 201–204 (1997). https://doi.org/10.1038/ng0297-201

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