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Genomic imprinting is an epigenetic phenomenon whereby the expression of a gene, chromosomal region, or entire chromosome, depends on the sex of the transmitting parent. Imprinting results in an otherwise fully functional gene being transcriptionally silenced when transmitted by one parent, yet the same gene, with identical DNA sequence, is active when transmitted by the other. Thus, the gene retains an imprint or “memory” of its genetic history, which is reversible and reset each successive generation by passage through the germline. Within this thesis, I present my findings that show genomic imprinting in Drosophila is regulated by distinct epigenetic mechanisms at different stages of embryogenesis, suggesting the requirement of a transitional stage to stabilize the imprint between establishment in the germline and maintenance in the soma. I futher show that Drosophila utilize epigenetic mechanisms that are involved in regulating genomic imprinting in mammals and plants, such as DNA methylation, histone modification, antisense RNA, and chromatin insulators. These findings demonstrate convergence of the epigenetic mechanisms that regulate genomic imprinting in diverse organisms.

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Several genes involved in the regulation of apoptosis can influence longevity. Although observations in several different systems imply that apoptosis and aging are closely linked, the relationship between the two remains largely unknown. In this study, Drosophila melanogaster was used as a model organism to explore the relationship between aging and apoptosis regulation. Apoptosis was investigated using two apoptotic hallmarks: caspase activity and DNA fragmentation. The results showed that apoptosis occured in adult flies at all ages and the changes in apoptosis associated with aging were linked to physiological age and were tissue-specific. During normal fly aging, apoptosis increased gradually within the muscle and was activated in the fat of old flies. However, neither of the two apoptotic signs were shown in the nervous system. The analysis of the apoptotic response to starvation and oxidative stress suggested that the increased apoptosis in muscle resulted from the accumulation of oxidative damage associated with aging. Once the presence of apoptosis during Drosophila aging was confirmed, the expression of anti-apoptotic genes was manipulated in specific tissues to examine the impact of a localized alternation of apoptosis on aging. The overexpression of anti-apoptotic genes in muscle extended Drosophila mean and maximum life span up to 99% and 65%, respectively. This extension was mediated by apoptosis inhibition using the detection of caspase activity and DNA fragmentation. In addition, the long-lived animals exhibited increased resistance to oxidative stress and preserved flight ability. Overall this study establishes that muscle apoptosis limits life span and participates in sarcopenia. This finding may have applications in the development of interventions to improve the life quality of elderly human. / Thesis (Ph.D, Biology) -- Queen's University, 2008-10-27 00:24:02.204

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Traditional screens for female sterile mutants have revealed only two genes which when mutant, give a fully penetrant 16 nurse cell phenotype. One way to gain a better understanding of the function of these genes in oocyte determination, is to identify genes which interact with them. Using P-element mutagenesis, I have isolated one dominant suppressor and five dominant enhancers of Bicaudal-D, and begun the phenotypic and molecular characterization of three of these genes. By deficiency screening, I have identified two different loci which act as dominant enhancers of Bic-D, and eight different loci which act as dominant suppressors of Bic-D. Further work on defining the locus responsible for the strong suppression phenotype associated with one of these deficiencies, revealed betaH-spectrin to be a strong dominant suppressor of loss-of-function Bic-D alleles, and a strong dominant enhancer of Bic-D gain-of-function alleles.