Thesis (Ph.D.)--University of Adelaide, Dept. of Animal Science, 2003. / "April 2002" Includes bibliographical references (leaves 200-249).

No description available.

Thesis (Ph. D.)--University of Texas at Austin, 2006. / Vita. Includes bibliographical references.

Thesis (Ph. D.)--University of Hong Kong, 2001. / Includes bibliographical references (leaves 154-172).

Thesis (Ph. D.)--University of Texas at Austin, 1999. / Vita. Includes bibliographical references (leaves 178-199). Available also in a digital version from Dissertation Abstracts.

No description available.

Recently, the timing of oocyte loss during murine development has been brought into question as authors using mouse vasa homologue (MVH) as a germ cell marker did not observe a loss of oocytes during fetal life. Instead the major loss was observed in the days following birth, after chromosome pairing has occurred. / In this study the controversy was addressed by establishing a new and reliable method to quantify murine oocytes in meiotic prophase, as well as to determine the gestation age and meiotic prophase stage of oocyte loss. Earlier limitations were overcome through the use of Germ Cell Nuclear Antigen-1 (GCNA-1) antibody as a germ cell specific marker, and the novel addition of a cytospin centrifugation step to the method. Progress through meiotic prophase was examined in chromosome spread preparations where meiotic stages were assessed using an antiserum against synaptonemal complex (SC) proteins. Quantification was accomplished by counting the number of GCNA-1 immunoreactive cells in chromosome spread preparations and estimated in histological sections using the ratio estimation model. (Abstract shortened by UMI.)

Early identification of mutant embryos prior to the manifestation of a defect facilitates the study of dysmorphogenesis. The In(l)lRk inversion was used as a cytogenetic marker to distinguish embryonic day 9 (D9) splotch (Sp) and splotch-delayed $(Sp sp{d})$ mouse mutants from heterozygous and wild-type littermates, and cellular aspects of abnormal neurulation and NCC migration were examined before inherent neural tube defects (NTDs) and deficiencies in neural crest cell (NCC) derivatives developed. In vitro analysis of NCC emigration from D9 neural tube explants revealed a delay in the release of NCCs from mutant neural tubes compared to controls, suggesting that the primary effect of the mutation was intrinsic to the neuroepithelium. Immunofluorescent localization of the neural cell adhesion molecule (N-CAM) antibody in situ demonstrated an increased intensity of antibody fluorescence in mutant tissue compared to controls, and further characterization by immunoblot analysis showed an altered embryonic N-CAM profile in both Sp and $Sp sp{d}$ mutants at D9 of gestation. The importance of N-CAMs in mediating cellular organization and communication has been well documented, supporting the idea that an alteration in this adhesion mechanism could result in the types of defects seen in splotch locus mouse mutants.

H1 histones are potentially significant to nuclear reprogramming during the oocyte-to-embryo transition. One characteristic distinguishing the H1 subtypes is that the somatic H1 histones are found primarily in dividing cells, whereas the H10 subtype is predominantly found in differentiated cells. The H1 complement in mouse oocytes and preimplantation embryos from wild-type and H10-/- animals was investigated. / Immunocytochemistry of wild-type cells demonstrated that H10 was predominant in oocytes while somatic H1 began accumulating in the 2-cell embryo. In H10-/- cells H10 was not detected, but, surprisingly, somatic H1 was detected beginning at the 1-cell stage. Radiolabeling of wild-type and H10-/- cells revealed that somatic H1 synthesis intensified after meiotic maturation, and therefore prior to its detection in embryos. The functional study found that loss of H10 impaired oogenesis but enhanced embryogenesis. The patterns of H1 immunodetection and synthesis are integrated, and the significance of H1 composition in development is discussed.

Cell adhesion molecules are known to play crucial roles in a variety of developmental processes. The neural cell adhesion molecule N-CAM is strongly implicated in neurulation and neural crest cell (NCC) migration and was thus studied in splotch (Sp) neural tube defect mutant embryos. At the 20 somite-stage of gestation day 9, Sp N-CAM was found to contain polysialic acid (PSA) side chains which are normally only present beginning at gestational day 11. Younger embryos at 12 and 14 somites also showed the presence of PSA on N-CAM, which was absent in controls. Enzymatic removal of PSA from N-CAM resulted in isoforms which migrated identically to PSA-free N-CAM isoforms in SDS-polyacrylamide gels. The post-translational modification of N-CAM appears to be the primary target of the Sp gene. In view of N-CAM's importance during development, an alteration at a critical stage is likely to result in the cascade of abnormalities seen in Sp mutants. / A new genotyping assay was also implemented for examination of N-CAM in Sp and other related wildtype strains.