Spermiogenesis in commercial poultry species: Anatomy and control

Spermatogenesis is a complicated process dependent upon several factors. Fo rmation of a testis requires the interaction of gene-products and hormones (androgens) on pluripotent tissue. In birds, the female is the heterogameti c (ZW) sex, but W chromosomal genes do not influence gonadal development in a way similar to the SRY gene on the mammalian Y chromosome. How ever; aut osomal genes such as SRY-like HMG box gene 9 (SOX9) may influence gonadal d evelopment. Hormones affect development; male gonads subjected to estrogen form an ovotestis, whereas ovaries exposed to aromatase inhibitors form an atypical testis. Sertoli cell numbers are set early in spermiogenesis, poss ibly under the influence of follicle-stimulating hormone and thyroid hormon e, and this may determine the number of genial cells that can be supported. Sertoli cells make a number of substances that affect testicular developme nt and function, particularly anti-Mullerian hormone, which inhibits female oviduct formation from the Mullerian anlage, inhibits aromatase activity t o stop estrogen production, and possibly stimulates androgen production by Leydig cells. Undifferentiated primordial germ cells (PGC) migrate to the t estis and are converted to spermatogonia by factors from gonadal ridge tiss ue and androgens. The PGC of males in the ovary form oocytes of Z genotype, whereas the female PGC in males form mostly Z sperm (with a few of W genot ype). Transmission electron microscopy micrographs of turkey testis are presented , and control of spermatogenesis by hormones and cytokines is discussed. Th is discussion includes follicle-stimulating hormone, luteinizing hormone, i nhibin, activin, follistatin, tumor necrosis factor-alpha, growth factors s uch as transforming growth factor-beta, interleukins, and interferon. Altho ugh information concerning paracrine and autocrine regulation of the avian testis by these substances is sparse, much can be learned from mammalian st udies, in which putative roles of each of these substances have been establ ished. How Sertoli cells cause directed apoptosis of spermatogonia using th e Fas-ligand, Fas-receptor pathway is reviewed, as well as ways to circumve nt this process. A possible role for ubiquitin concerning prevention of hea t-induced damage to the testis is presented.