Cellular interactions in the mammalian ovarian follicle between its germ‐line and somatic cell components are crucial for its development and function. These interactions are mediated by both membrane gap junctions and paracrine factors. Somatic cell‐to‐oocyte communication is essential for oocyte growth and the regulation of meiotic maturation. In particular, granulosa cells provide nutrients and molecular signals that regulate oocyte development. Oocytes, on the other hand, promote the organization of the follicle, the proliferation of granulosa cells, and the differentiation (...) and function of cumulus cells, a subset of granulosa cells. Determining the nature of the oocyte‐to‐granulosa cell signals remains a key challenge for future work. (shrink)

The oocyte is not only the rarest and the largest cell in the body, but it also has one of the most remarkable life histories. Formed in the fetal ovary and suspended at diplotene of meiosis, it may wait for years before beginning to grow, and not until this process is complete can it resume meiosis and undergo fertilisation. Major changes in the number, morphology and distribution of cytoplasmic organelles occur during growth, and a molecular program for embryogenesis is formed. (...) Specific yolk proteins are absent and much of the RNA and some of the protein are degraded by the cleavage stage. The zona pellucida has been intensively studied, but knowledge of oocyte‐specific genes is otherwise surprisingly patchy given the significance of this cell type and the expansion of reproductive technology. Finally, it is now clear that oocytes are not mere passengers which depend on granulosa cells for nutrition and regulation but actively promote the growth and differentiation of their follicles. (shrink)

Until recently, sex determination in mammals has often been described as a male determination process, with male differentiation being the active and dominant pathway, and only in its absence is the passive female pathway followed. This picture has been challenged recently with the discovery that the gene encoding R-spondin1 is mutated in human patients with female-to-male sex reversal.((1)) These findings might place R-spondin1 in the exceptional position of being the female-determining gene in mammals. In this review, possible roles of R-spondin1 (...) during sex determination as well as questions arising from this study will be discussed. (shrink)