From germ cell to fertilizable oocyte is a journey that captures the essence of MHR: a quest to understand the basic science of reproductive medicine. In view of the rapid developments in molecular biology and genetics, a major goal of ESHRE in recent years has been to provide clinicians, counsellors, embryologists and the public with novel research findings of relevance to assisted reproduction technologies (ART). In this spirit, the ESHRE Campus workshop in Potsdam in October 2009 on

more »

... n Folliculogenesis and Oogenesis: from basic science to the clinic' was dedicated to fundamental research in an area that is increasingly affecting clinical practice. The meeting was well attended (Fig. 1 ) and eight invited speakers submitted manuscripts for peer review and collation into this thematic issue of MHR, the key messages of which are highlighted below. Møllgård et al. (2010) open with a novel perspective on how human primordial germ cells (PGCs) first visible in the wall of the embryonic yolk sac might migrate to the hindgut and the primitive gonads. On the basis of an elegant series of immunocytochemical and electron microscopic observations, they posit that a majority of PGCs remain at the proximal end of the yolk sac, which becomes part of the wall of the hind-and midgut close to where the gonads develop. PGCs do not therefore have to move very far in order to reach the gonadal ridges. The idea is that PGCs migrate from there to the primitive gonad by tracking autonomic nerve fibres and Schwann cells extending across the dorsal mesentery to the gonadal ridge. The invoked pathfinder function of these cells might be explained by their release of chemo-attractants and/or transmit survival signals that may support and guide PGC migration from the hindgut to the gonads. De Felici (2010) revisits the controversial issue of mammalian neo-oogenesis, speculating how germ stem cells (GSCs) found in the ovary after birth might be derived from somatic cells, PGCs or PGC-derived GSCs formed before birth. Such cells that commence-but do not complete-programming into germ cells during early embryogenesis may be retained into adulthood, providing precursors for 'neo-oogenesis' under certain (e.g. stress-related) conditions later on. However, as De Felici (2010) concedes, crucial evidence for the progression of such stem cells to fully competent oocytes in an adult ovary is absent. Moreover, there is still no compelling evidence that neo-oogenesis occurs naturally or is inducible in mammals. Turning to the initiation of follicular growth, Nielsen et al. (2010) spotlight the TGF-beta superfamily member Anti-Mullerian Hormone (AMH), which is produced by follicular epithelial (granulosa) cells. They report that AMH concentration in follicular fluid and granulosa cell mRNA expression of CYP19 (encoding the aromatase enzyme essential for estrogen synthesis) are negatively correlated in human small antral follicles, consistent with a suppressive paracrine effect of AMH on follicular development. However, since AMH recep-tor2 (AMH-r2), follicle-stimulating hormone receptor 2 (FSH-r) and CYP19 mRNA are all positively associated, the role of AMH in follicular development and steroidogenesis remains enigmatic. Folliculogenesis is a protracted process in humans requiring several months from primordial follicle recruitment to large antral follicle formation and ovulation. Activin, another member of the TGF-beta family of growth factors produced by granulosa cells, is known to modulate FSH action during pre-antral follicle development. McLaughlin et al. (2010) investigate the interaction of activin and FSH on bovine cultured pre-antral follicles as a model for humans. They provide evidence that activin treatment alone or with FSH promotes oocyte growth, through increasing connexin 43 gap junctional expression in a polarized fashion (i.e. at the oocyte/granulosa cell interface and at the follicular periphery); thereby activin supports granulosa cell anchorage to the follicle wall (basement membrane) as well as the zona pellucida of the oocyte. This previously unknown property of activin could have translational implications for the improvement of clinical in vitro maturation culture protocols. The final step in follicular maturation leading to release of a fertilizable oocyte depends on the ovulation-inducing Luteinising Hormone (LH) surge. The mini-review by Solc et al. (2010) surveys the signalling pathways through which LH triggers meiotic resumption. These involve paracrine signalling via epidermal growth factor (EGF)-like proteins produced in mural granulosa cells should lead to reduced cGMP formation in cumulus cells. Since cGMP inactivates phosphodiesterase 3a (PDE3a) in the oocyte the reduction in cGMP in turn causes PDE3a activation and cAMP decrease. The attendant cAMP decrease orchestrates the downstream signalling network that switches on the CDK1/ CyclinB (MPF) 'master switch', to resume meiosis. Vogt et al. (2010) focus on the M-phase to anaphase I transition during meiotic maturation. Their work emphasizes Aurora kinase B