Endocrine Regulation of Spermatogenesis in Teleost Fish

Abstract

Mitotic proliferation of spermatogonia, meiosis of spermatocytes, and the restructuring of round spermatids into flagellated spermatozoa (spermiogenesis), are hallmark events of spermatogenesis. The process is fuelled by stem cells that either self-renew or produce spermatogonia committed to further development. Germ cells always require the close contact with Sertoli cells. These somatic cells, but not germ cells, express receptors for androgens and follicle-stimulating hormone (FSH), thus functioning as interface between hormones and the developing germ cells. In Japanese eel, for example, gonadotropin of 11-ketotestosterone (11-KT; a typical androgen in fish) stimulation induces complete spermatogenesis ex vivo, and spermatogonial proliferation is in part mediated by Sertoli cell-derived activin. In fish LH, but also FSH, stimulates steroidogenesis. Since FSH but not LH circulates in sexually immature salmonids, increased FSH signalling may be sufficient to initiate spermatogenesis by activating both Sertoli cell functions and 11-KT production. Fish testes also produce testosterone (T), which exerts negative feedback effects on FSH-dependent signalling and on steroidogenesis. The balance between T and 11-KT production and plasma levels therefore is important. Besides inducing spermatogonial proliferation, 11-KT also induces meiosis and complete spermiogenesis in tissue culture. However, it is not known yet by what mechanisms 11-KT stimulates the passage of germ cells through these more advanced stages of development.