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Title page for ETD etd-11292010-123006

Type of Document Dissertation
Author LaFever, Leesa Marie
Author's Email Address punchbug4u@yahoo.com
URN etd-11292010-123006
Title The role of diet in the regulation of Drosophila ovarian stem cells and their progeny
Degree PhD
Department Cell and Developmental Biology
Advisory Committee
Advisor Name Title
Chin Chiang, Ph.D. Committee Chair
Daniela Drummond-Barbosa, PhD Committee Member
Jim Goldenring, MD PhD Committee Member
Laura Lee, MD PhD Committee Member
Lila Solnica-Krezel, PhD Committee Member
  • adipocytes
  • oogenesis
  • nutrition
  • ovarian stem cells
  • Reproduction
  • adipokine signaling
Date of Defense 2010-10-22
Availability unrestricted
Adult stem cells respond to environmental signals, such as diet, to properly maintain tissues; however, the mechanisms involved are largely unknown. The Drosophila ovary is a stem cell-based tissue that responds dramatically to diet, has a well-defined cell biology and is one of the premier systems for the study of stem cell regulation in vivo. In this thesis I examine the roles of insulin and Target of rapamycin (TOR) signaling in regulating Drosophila ovarian stem cell proliferation and maintenance, and the growth, proliferation, and survival of their progeny. Although insulin and TOR signaling both play cell-specific roles in regulating how stem cells and their progeny respond to diet, evidence suggests that other factors, potentially from fat cells, are also required. One potential mechanism by which fat cells may communicate nutritional status to the ovary is via adipokine-like signaling. In mammals, the adipokine adiponectin binds its receptors on peripheral tissues, sensitizing them to insulin signaling. Drosophila has an adiponectin receptor (dAdipoR) homolog that, according to my preliminary results, appears to have a cell-autonomous, diet-dependent role in regulating GSC maintenance and the proliferation of their progeny. Furthermore, fat-cell knockdown of dAdipoR increases the number of divisions during germline cyst formation, suggesting that dAdipoR-mediated signaling in multiple tissues modulates oogenesis. To identify potential dAdipoR ligands and/or additional fat cell factors that link fat cell nutrient-sensing to ovarian stem cell regulation, I took a quantitative proteomics approach to identify fat cell secreted proteins regulated by diet. A fat cell-specific RNAi assay will be used to determine which fat body secreted candidates have a role in ovarian stem cell regulation. These studies provide key insights into the highly conserved regulatory mechanisms that control the stem cell response to diet and suggest that multiple factors, likely from multiple tissues, together act to coordinate stem cell activity with the nutritional demands of an organism.
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