Follistatin suppresses FSHβ but increases LHβ expression in the goldfish – evidence for an activin-mediated autocrine/paracrine system in fish pituitary

Abstract

Our previous study demonstrated that recombinant goldfish activin B stimulated goldfish FSHβ but inhibited LHβ expression. Similar to activin B, activin A also exhibited the inverse effects on the expression of the two gonadotropins. The novel dual effects of activins on FSH and LH in the goldfish raise an interesting question as to where the activin comes from in vivo. In the present study, we first demonstrated the expression of activin, its receptors and binding protein follistatin in the goldfish pituitary, leading to a suggestion that an autocrine/paracrine regulatory system involving activin is operative in fish pituitary. To investigate the functionality of the pituitary-derived activin system in the regulation of gonadotropin biosynthesis, we further examined the effects of follistatin, an activin-binding protein, on goldfish FSHβ and LHβ expression. Follistatin not only reversed the effects of exogenous activin on FSHβ and LHβ expression but also had inverse effects on the basal expression of the genes; and its effects were opposite to those of activin. This suggests that the endogenous activin plays roles in controlling the expression of both FSHβ and LHβ genes. It is conceivable that any factors that influence the intrapituitary activin system in vivo will likely affect the biosynthesis of the two gonadotropins in the goldfish.