Spermatogenesis-preventing substance

Spermatogenesis, the formation of sperm, is a complex developmental process that begins with the mitotic proliferation of spermatogonia and proceeds through extensive morphological changes that convert the haploid spermatid into a mature, functional spermatozoon. Although the process of spermatogenesis is the same in both mammalian and nonmammalian vertebrates, its control mechanisms are not well understood. In higher vertebrates, it is difficult to analyse the control mechanisms of spermatogenesis because the seminiferous tubules contain several successive generations of germ cells (Clermont, 1972), and few culture systems are available for induction of spermatogenesis in vitro (Abe, 1987). Various reproductive styles and gametogenetic patterns exist among species of teleost. Japanese eel, for example, has a specific spermatogenetic pattern. Under fresh-water culture conditions, the male Japanese eel has immature testes containing only non-proliferated type A and early type B spermatogonia (Miura et al., 1991a). It has been reported, however, that human chorionic gonadotropin (hCG) injection can induce all stages of spermatogenesis in vivo (Miura et al., 1991a). Furthermore, Japanese eel is the only animal in which complete spermatogenesis has been induced by hormonal treatment in vitro using an organ culture system and a germ cell/somatic cell co-culture system (Miura et al., 1991b; Miura et al., 1991c; Miura et al., 1996). Thus, the eel testis provides an excellent system for studying the regulation of spermatogenesis. Using these in vivo and in vitro systems in the eel, the following control mechanisms of spermatogenesis have been identified. The hormonal induction of spermatogenesis in eel testes is mediated via gonadotropin stimulation of Leydig cells, which produce 11-ketotestosterone (Miura et al., 1991a; Miura et al., 1991b). In turn, 11-ketotestosterone induces complete spermatogenesis from spermatogonia to spermatozoa through the action of Sertoli cells (Miura et al., 1991c). However, many details of this pathway remain unresolved. In particular, it seems that there are complex control mechanisms related to the initiation of spermatogenesis after 11-ketotestosterone stimulation. It seems likely that key factors involved in the initiation of spermatogenesis are either expressed or suppressed by 11-ketotestosterone during hCG-induced spermatogenesis. Specifically, suppressive factors might have an inhibitory effect 2689 Development 129, 2689-2697 (2002) Printed in Great Britain © The Company of Biologists Limited 2002 DEV3628