An unusually high level of inter- and intraspecific variability in spermatozoa has been well documented. However, recent evidence indicates that the level of variation within spermatozoa differs markedly across taxa. In particular, it appears that the variability in spermatozoa tends to decrease across species as the risk of sperm competition increases. In this thesis, I present a model that explains how variability in spermatozoa may arise due to errors made during the sperm production process. In doing so, I also provide an explanation for why variability in sperm traits tends to decrease as the level of sperm competition experienced by males of a given species increases. The model presented in this study provides a novel perspective on spermatozoa and their production. While many sperm traits are thought to be selected upon, I suggest that variability in spermatozoa may also be the result of evolutionary forces such as sperm competition. Variability in spermatozoa, then, can be adaptive and can represent an optimal reproductive strategy. / Thesis (Master, Biology) -- Queen's University, 2009-09-25 21:53:23.172

No description available.

<p>Gonadotropin Releasing Hormone (GnRH) is a hypothalmic decapeptide, which regulates mammalian gonadotropin secretions by binding to specific, high affinity receptors in the pituitary. Two forms of GnRH (GnRH I and GnRH II) are expressed in the brain of human and some primates. Even though primates have been used extensively in a variety of investigations in relation to the role of GnRH in reproduction, there is no evidence of any research to investigate the direct effect of GnRH on primate sperm.</p>

<p>Gonadotropin Releasing Hormone (GnRH) is a hypothalmic decapeptide, which regulates mammalian gonadotropin secretions by binding to specific, high affinity receptors in the pituitary. Two forms of GnRH (GnRH I and GnRH II) are expressed in the brain of human and some primates. Even though primates have been used extensively in a variety of investigations in relation to the role of GnRH in reproduction, there is no evidence of any research to investigate the direct effect of GnRH on primate sperm.</p>

Research Doctorate - Doctor of Philosophy / On leaving the testis, spermatozoa can neither swim nor fertilize the oocyte. These functional properties are acquired as spermatozoa engage in a process of post-testicular maturation in the epididymis. The studies described in this thesis were designed to elucidate some of the fundamental mechanisms associated with the regulation of epididymal maturation in mouse spermatozoa. The initial studies described in this thesis investigated the expression of a cAMP/PKAdependent, tyrosine phosphorylation signaling pathway that becomes activated during epididymal sperm maturation. It was demonstrated that the entry of spermatozoa into the epididymis was accompanied by the sudden stimulation of this pathway, initially in the principal piece of the cell and subsequently in the midpiece. The competence of these cells to phosphorylate the entire sperm tail, particularly the mitochondria, was accompanied by a capacity to exhibit hyperactivated motility on stimulation with cAMP. A distinctly different pattern of tyrosine phosphorylation involving the acrosomal domain of the sperm head was provoked as spermatozoa entered the caput epididymis and then remained high until these cells entered the distal corpus and cauda. However, tyrosine dephosphorylation of the sperm acrosomal domain during epididymal transit did not appear to be functionally involved in controlling the acrosome reaction. Research into the biochemical basis of sperm epididymal maturation revealed that this process was associated with the activation of sperm mitochondria, leading to the creation of a mitochondrial membrane potential (MMP) and activation of mitochondrial free radical generation. Immature caput spermatozoa displayed a low MMP whereas mature caudal spermatozoa actively maintained a high MMP. Moreover mitochondrial generation of reactive oxygen species (ROS) could be triggered by antimycin A in mature caudal spermatozoa but not in immature caput spermatozoa, suggesting a lack of electron flux in the latter. The molecular mechanisms responsible for regulating mitochondrial function were also found to be reversible, as washing the cells free of epididymal fluid allowed caput spermatozoa to acquire a high MMP and generate ROS while incubating caudal spermatozoa in caput epididymal fluid, suppressed MMP and their ability to generate ROS. Pharmacological suppression of mitochondrial activity was subsequently found to be associated with the inhibition of hyperactivated motility. These results strongly suggested that fluid from the caput epididymis contained a mitochondrial inhibitor and that activation of mitochondrial activity was due to the removal or inactivation of this inhibitor during epididymal transit. This causative factor was not species specific. Incubation of ejaculated human spermatozoa in murine epididymal fluid systematically suppressed their MMP. The characterization of caput epididymal fluid suggested that the putative mitochondrial inhibitor is a heat-resistant protein with a molecular weight larger than 30 kDa. The final results presented in this thesis demonstrate that a full-length Riken protein is a potential candidate for the putative mitochondrial inhibitor that switches off mitochondrial function in caput spermatozoa. Indeed, these results represent the first report suggesting that the epididymal maturation is associated with activation of sperm mitochondria and the first study of a testis specific protein that could be a regulator of mitochondrial function in the male germ line. Further characterization of the mechanisms by which epididymal spermatozoa control mitochondrial function may hold the key to our understanding of sperm maturation. It may also lead us to a clear exposition of the molecular basis of human male infertility, potentially serve as a target for infertility treatment and possibly contribute to the development of novel contraceptive agents.

Thesis (MScMed)--University of Stellenbosch, 2005. / Bibliography. Also available via the Internet.

Diss. (sammanfattning) Uppsala : Sveriges lantbruksuniversitet, 2005. / Härtill 4 uppsatser.

Thesis (Ph.D.) -- University of Adelaide, Dept. of Obstetrics and Gynaecology, 1999. / Errata posted inside back end-paper (leaf 250). Bibliography: leaves 204-249.

Thesis (M.Sc. (Anatomy))--Mahidol University, 1984.

Thesis (Ph.D. (Biochemistry))--Mahidol University, 1982.