The biology of spermatogenesis: the past, present and future

Abstract

The physiological function of spermatogenesis in Caenorhabditis elegans, Drosophila melanogaster and mammals is to produce spermatozoa (1n, haploid) that contain only half of the genetic material of spermatogonia (2n, diploid). This half number of chromosomes from a spermatozoon will then be reconstituted to become a diploid cell upon fertilization with an egg, which is also haploid. Thus, genetic information from two parental individuals can be passed onto their offspring. Spermatogenesis takes place in the seminiferous epithelium of the seminiferous tubule, the functional unit of the mammalian testis. In mammals, particularly in rodents, the fascinating morphological changes that occur during spermatogenesis involving cellular differentiation and transformation, mitosis, meiosis, germ cell movement, spermiogenesis and spermiation have been well documented from the 1950s through the 1980s. During this time, however, the regulation of, as well as the biochemical and molecular mechanisms underlying these diverse cellular events occurring throughout spermatogenesis, have remained largely unexplored. In the past two decades, important advancements have been made using new biochemical, cell and molecular biology techniques to understand how different genes, proteins and signalling pathways regulate various aspects of spermatogenesis. These include studies on the differentiation of spermatogonia from gonocytes; regulation of spermatogonial stem cells; regulation of spermatogonial mitosis; regulation of meiosis, spermiogenesis and spermiation; role of hormones (e.g. oestrogens, androgens) in spermatogenesis; transcriptional regulation of spermatogenesis; regulation of apoptosis; cell -cell interactions; and the biology of junction dynamics during spermatogenesis. The impact of environmental toxicants on spermatogenesis has also become an urgent issue in the field in light of declining fertility levels in males. Many of these studies have helped investigators to understand important similarities, differences and evolutionary relationships between C. elegans, D. melanogaster and mammals relating to spermatogenesis. In this Special Issue of the Philosophical Transactions of the Royal Society B: Biological Sciences, we have covered many of these areas, and in this Introduction, we highlight the topic of spermatogenesis by examining its past, present and future.

Autophagy regulates spermatid differentiation via degradation of PDLIM1

“…The efficient cytoplasm removal is thought to be critical for the generation of functional and motile spermatozoa, but the mechanisms underlying this process remain poorly understood. 29 For a long time, the elimination of residual bodies was thought to be a passive process, and they were thought to be engulfed by the Sertoli cells. 30 However, the role of the spermatocytes themselves is largely ignored.…”

The evolutionary ecology of testicular function: size isn't everything

“…While reproductive and developmental biologists are making substantial progress in understanding spermatogenesis in a number of model species (e.g. Fuller, 1998;Kerr, Loveland & O'Bryan, 2006;White-Cooper, Doggett & Ellis, 2009;Cheng & Mruk, 2010;White-Cooper & Bausek, 2010), we often lack an ecological and evolutionary context in which to interpret these findings. Conversely, we generally know little about spermatogenesis in the diverse range of non-model organisms that tend to be the subject of evolutionary and ecological research on male reproductive investment and sperm competition.…”

Testin and actin are key molecular targets of adjudin, an anti-spermatogenic agent, in the testis

“…The most obvious phenotype following administration of adjudin to adult rats is the loss of developing germ cells from the seminiferous epithelium, most notably elongating/elongated spermatids, followed by round spermatids and spermatocytes but not spermatogonia residing outside of the BTB. 1,2,6 This leads to a transient loss in fertility; fertility is restored after spermatogonia reinitiate germ cell proliferation and differentiation and cells repopulate the seminiferous epithelium. 6 While adjudin is known to exert its initial effects at the apical ectoplasmic specialization (apical ES, a testis-specific anchoring junction found between Sertoli cells and step [8][9][10][11][12][13][14][15][16][17][18][19] spermatids in the rat testis), the molecular target(s) of adjudin remains unknown.…”

“…1,2 In contrast to hormonal approaches which disrupt spermatogenesis by interfering with the hypothalamic-pituitary-testicular axis, [3][4][5] adjudin exerts its effects behind the blood-testis barrier (BTB) in a specialized microenvironment known as the adluminal compartment. The most obvious phenotype following administration of adjudin to adult rats is the loss of developing germ cells from the seminiferous epithelium, most notably elongating/elongated spermatids, followed by round spermatids and spermatocytes but not spermatogonia residing outside of the BTB.…”