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This dissertation, Leptin Expression in Embryos Sired by Male Golden Hamsters (mesocricetus Auratus) With All Accessory Sex Glands Removed by Subin, Liao, 廖素彬, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Abstract of thesis entitled Leptin expression in embryos sired by male golden hamsters (Mesocricetus auratus) with all accessory sex glands removed Submitted by LIAO SUBIN for the degree of Doctor of Philosophy at The University of Hong Kong in August 2007 Leptin, the ob gene product, is mainly produced by adipose tissue with the primary function of regulating energy expenditure and metabolism. Recently, leptin is widely reported to play important roles in male and female fertility. In the female, leptin takes part in the preimplantation embryonic development, implantation process, fetal and placental development. Activation of the ob gene is regulated by DNA methylation in the promoter region where the DNA methyltransferase is involved. The regulation of DNA methylation is essential for normal embryonic development. Our previous study showed the removal of paternal accessory sex glands (ASGs) affects the subsequent embryonic development. Up to date, mechanism by which this effect extends from the sperm to subsequent embryos is not clear. The sperm genome is tightly packaged with protamine which is not easy to be modified during such a short period between ejaculation and fertilization. The epigenetic remarks are more likely to alter the DNA methylation and passed onto the subsequent embryos i sired and this may cause abnormalities in embryonic development. In the present study, leptin in sperm and seminal plasma of male golden hamsters with or without ASGs removed were measured by immunofluorescent staining and ELISA. Before ejaculation, epididymal sperm contains leptin. After ejaculation, leptin was added from the ASG secretions. Leptin was lower in sperms and seminal plasma from the group with ASGs removed. This showed that ASGs secrete leptin and the removal of ASGs lowered the leptin in sperm. The polarized leptin expression pattern in the oocytes and preimplantation embryos suggested the relationship with the cleavage plane and formation of the animal pole in the embryos. At 4-cell stage, leptin immunofluorescent signal in the TX group (paternal ASGs removed) was lower than that of normal control. Differing from the mouse, ob mRNA in the golden hamster was not detected in the preimplantation embryos. We found initial leptin expression in 6 dpc embryos at implantation stage by in situ hybridization. The removal of paternal ASGs affected the development of embryos sired. During midgestation, at 11 dpc, a lower fetal weight and leptin level were found. The higher methylation status in the leptin promoter in 11 dpc stage TX embryos ii detected by bisulfite sequencing PCR suggested the removal of paternal ASGs lowered demethylation rate in the embryos sired. The higher level of Dnmt1 (DNA methyltransferase) immunostaining signal in the 11 dpc embryos gave evidence that removal of paternal ASGs may alter the DNA methylation through the DNA methyltransferase change. In conclusion, work in this thesis demonstrated that the lack of exposure of sperm to accessory sex gland secretions influenced the demethylation rate in the ob promoter and affected leptin expression in midgestation embryos sired, and resulted in delayed embryonic development. This study reports that ob is a gene regulated by paternal factors to control the fetal development and that paternal ASG secretion contain factors that affect the

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