Abstract
Spermatogenesis is a complicated process dependent upon several factors. Formation of a testis requires the interaction of gene-products and hormones (androgens) on pluripotent tissue. In birds, the female is the heterogametic (ZW) sex, but W chromosomal genes do not influence gonadal development in a way similar to the SRY gene on the mammalian Y chromosome. However, autosomal genes such as SRY-like HMG box gene 9 (SOX9) may influence gonadal development. 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, possibly under the influence of follicle-stimulating hormone and thyroid hormone, and this may determine the number of gonial cells that can be supported. Sertoli cells make a number of substances that affect testicular development and function, particularly anti-Mullerian hormone, which inhibits female oviduct formation from the Mullerian anlage, inhibits aromatase activity to stop estrogen production, and possibly stimulates androgen production by Leydig cells. Undifferentiated primordial germ cells (PGC) migrate to the testis and are converted to spermatogonia by factors from gonadal ridge tissue 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 genotype). Transmission electron microscopy micrographs of turkey testis are presented, and control of spermatogenesis by hormones and cytokines is discussed. This discussion includes follicle-stimulating hormone, luteinizing hormone, inhibin, activin, follistatin, tumor necrosis factor-alpha, growth factors such as transforming growth factor-beta, interleukins, and interferon. Although information concerning paracrine and autocrine regulation of the avian testis by these substances is sparse, much can be learned from mammalian studies, in which putative roles of each of these substances have been established. How Sertoli cells cause directed apoptosis of spermatogonia using the Fas-ligand, Fas-receptor pathway is reviewed, as well as ways to circumvent this process. A possible role for ubiquitin concerning prevention of heat-induced damage to the testis is presented.
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