The present thesis provides information regarding the endocrine and paracrine regulation of zebrafish spermatogenesis that is relevant to both, academic and applied interests. New knowledge has been obtained with respect to the functions of Fsh-regulated factors, produced by Sertoli- and Leydig cells, in regulating spermatogonial development in the zebrafish. Our main findings highlight the endocrine effects of Fsh and T3 on promoting zebrafish spermatogenesis by regulating paracrine signalling molecules such as Igf3 and its binding proteins, Insl3 and Amh, which in turn modulate spermatogonial proliferation and differentiation. Amh counteracts stimulatory actions, i.e. by blocking Fsh-androgen production (Skaar et al., 2011) and Igf3-stimulated spermatogonial proliferation and differentiation, or by promoting inhibin expression or prostaglandin E2 production, which in turn prevent germ cell differentiation.
Overall, there are apparently two completely independent ways of how spermatogenesis can be supported in fish: one having Fsh stimulating Leydig cell androgen production, which can support full germ cell development without significantly modulation of growth factor [removed]Assis et al., 2018) and, another one having Fsh stimulating a range of Sertoli- and Leydig cell-derived growth factors and other local regulators (e.g. PGE2) that exert more targeted effects compared to the broad activity of androgens. In this context, Fsh plays a central role in regulating testis physiology leaving much room for future work to learn how reproductive hormones control spermatogenesis. This thesis also suggests that the zebrafish model is not only suitable for basic research on the regulation of stem cell activity but also of potential value for solving reproduction-related problems in aquaculture species, e.g. salmon.