Endocrine Abstracts

It is now possible to modify the mouse genome to generate strains of mice with precise genetic mutations. Over 50 strains of mutant mice have now been produced in which there is an alteration in female fertility (Elvin and Matzuk, Reviews of Reproduction, 1998). For example, we have shown that a knockout of the oocyte-specific TGF-beta family member, growth differentiation factor-9 (GDF-9), results in a block at the primary follicle stage (Dong et al., Nature, 1996; Carabatsos et al., Developmental Biology, 1998; Elvin et al., Molecular Endocrinology, 1999a), and recombinant GDF-9 can substitute for the oocyte to regulate genes which are spatiotemporally expressed in the preovulatory ovarian follicle (Elvin et al., Molecular Endocrinology, 1999b, Elvin et al., Proc Natl Acad Sci USA 2000). Additionally, mice lacking FSHβ are infertile due to a block at the preantral-antral stage transaction (Kumar et al., Nature Genetics, 1997). Our laboratory is continuing to focus on the functional characterization of these proteins and additional oocyte-specific gene products as possible novel fertility and contraceptive targets.