Thesis (Ph.D.)--University of Melbourne, Depts. of Paediatrics and Public Health, 2005. / Typescript. Includes bibliographical references (leaves 271-283).

Thesis (Ph. D.)--Johns Hopkins University, 2005. / Includes bibliographical references (p. 185-204).

No description available.

Thesis (Ph.D.)--Drexel University, 2007. / Includes abstract and vita. Includes bibliographical references (leaves 157-200).

Thesis (M.S.)--University of North Carolina at Greensboro, 2007. / Title from PDF title page screen. Advisor: John Tomkiel; submitted to the Dept. of Biology. Includes bibliographical references (p. 58-62).

Proper regulation of sleep and metabolism are critical to the survival of all organisms. In humans, dysregulation of sleep is linked to metabolic syndrome, including hypertension, hyperglycemia and hyperlipidemia. However, the mechanisms regulating interactions between sleep and metabolism are poorly understood. Although the fruit fly, Drosophila melanogaster, bears little anatomical resemblance to humans, it shares similar genetics essential in understanding normal development and disease in humans. From humans to flies, many disease-related genes and pathways are highly conserved, rendering the fruit fly ideal to understanding the interactions between sleep and metabolism. Therefore, using the fruit fly provides a framework for understanding how genes function between sleep and metabolism. During starvation, both humans and rats reduce their sleep. Similarly, previous studies have shown that fruit flies also suppress sleep to forage for food, further showing that sleep and metabolism are intricately tied to one another and that they are highly conserved across species. To further explore the interactions between sleep and metabolism, I have conducted multiple genetic screens to identify novel regulators of sleep-metabolism interactions. These experiments led to the identification of the mRNA binding protein translin (trsn) as being required for starvation-induced sleep suppression. A second screen that targeted metabolic genes from a genome-wide association study identified the ion channel accessory protein uncoordinated 79 (unc79) as a critical regulator of both sleep duration and starvation resistance. The genes function in different regions of the brain and suggest complex neural circuitry is likely to underlie regulation of sleep metabolism interactions. Taken together, a mechanistic understanding of how different genes function to regulate sleep in flies will further our understanding of how sleep and metabolism is regulated in humans. / Includes bibliography. / Dissertation (PhD)--Florida Atlantic University, 2021. / FAU Electronic Theses and Dissertations Collection

Polycomb Group (PcG) proteins are responsible for post-transcriptional modifications in histone tails leading to chromatin condensation and changes in gene expression. In Arabidopsis thaliana, curly leaf (CLF) is a member of the Polycomb Reporssive Complex 2 (PRC2), which cnfers a repressive epigenetic mark, namely trimethylation of histone H3 at lysine 27 (H3K27me3). In the clf mutant, the expression of the floral organ identity gene AGAMOUS (AG) is derepressed in vegetative stages and coincides with loss of H3K27me3 at the AG locus. Recent whole genome prfiling studies have suggested that PcG genes regulate mang more developmental regulators than AG (about 15% of Arabidopis genes). However, it remains unclear what the relevance of PcG regulation of these targets is for plant development; in addition, it is not known how changes in J3K27me3 casue gene repression in plants. To unravel the role of CLFcin A. thaliana, a T-DNA mutagenesis in the clf background was performed to identify mutations enhancing or suppressing the Clf- phenotype, as these may identify additional PcG genes and targets. Firstly, I screened an A. thaliana T-DNA mutagenized population and identified four mutations suppressing the Clf- phenotype: suppressor of polycomb 1 to 4 (sop1, sop2, sop3 and sop4). Secondly, I characterized these four mutants. The sop1 mutant had normal flowering time and the suppressed phenotype is due to a loss of function mutation in SEPALLATA3 (SEP3). I establied the SEP3 is an activator and a co-factor of AG. Also, I found that SEP3 is stronlgy mis-expressed in clf mutants and SEP3 chromatin is enriched the H3K27me3, which stronly suggests that SEP3 is a direct target of CLF. In addition, I showed that a mutation in Flowering Locus T (FT), which is a positive regulator of SEP3, suppreesed the Clf- phenotype suggesting the FT is also a target of CLF. Suppressors sop3, sop3 and sop4 are late flowering, unlike sop1, and show increased expression of Flowering Locus C (FLC), a MADS-box transcription factor gene that represses flowering. I found that the sop4 mutation in likely casued by disruption of FPA, a predicted RNA binding protein that promotes flowering time by repressing FLC. Consistent with this, sop4 mutants show hight levels of FLC. Unexpectedly, fpa clf (sop4) mutatns are much later flowering than clf FRI mutants, which have similarly high levels of FLC. This suggests that FPA may regulate other genes controlling flowering thant FLC. The genes involved in sop2 and sop3 mutants remain to be identified. In this thesis I brought genetic and molecular evidence showing that CLF, though the PRC2, control floral induction (FLC), floral integration (FT) and floral organ formation (SEP3 and AG) in A. thaliana.

Thesis--University of Oklahoma. / Includes bibliographical references.

Thesis (Master of Health Policy and Administration)--Washington State University, May 2009. / Title from PDF title page (viewed on June 5, 2009). "Department of Health Policy and Administration." Includes bibliographical references (p. 34-39).

Thesis (Ph.D.)--University of Melbourne, Dept. of Paediatrics, Faculty of Medicine, Dentistry and Health Sciences, 2010. / Typescript. Includes bibliographical references (p. 101-111)