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The Drosophila aging process is affected by an array of factors including, but not
limited to, oxidative and heat-shock stress responses, insulin/IGF-1 signaling pathway,
dietary restriction (DR), and stem cell maintenance.
Oxidative stress response has long been known to be involved in the aging process. As
respiration occurs, oxygen is metabolized, and reactive oxygen species (ROS) are
inevitably released by mitochondria as a by-product. ROS have deleterious effects in
most tissues and are generally suppressed by various endogenous enzymes, including
superoxide dismutase (SOD) and catalase. Over-expression of these enzymes is
sometimes effective to extend Drosophila lifespan (Sun and Tower 1999; Sun, Folk et
al. 2002; Sun, Molitor et al. 2004). Heat-shock proteins have also been shown to be
beneficial for lifespan extension via increased stress resistance (Morrow, Samson et al.
2004; Wang, Benzer et al. 2004). Among the most investigated heat-shock proteins are
Hsp22 and Hsp23, where expression level correlates with life span (Kurapati, Passananti
et al. 2000).
The Insulin/IGF-1 pathway is conserved among various organisms including C.elegans
and Drosophila (Giannakou and Partridge 2007). Functionally conserved components in
this pathway include the insulin receptor (InR), phosphoinositide 3-kinase (PI3K) and
the forkhead transcription factor dFOXO. When certain critical components in the
insulin/IGF-1 pathway are knocked down, such as IGF receptor or the receptor substrate
Object Description
| Title | Characterization of Drosophila longevity and fecundity regulating genes |
| Author | Li, Yishi |
| Author email | yishili@usc.edu; yishili@gmail.com |
| Degree | Doctor of Philosophy |
| Document type | Dissertation |
| Degree program | Molecular & Computational Biology |
| School | College of Letters, Arts and Sciences |
| Date defended/completed | 2008-08-19 |
| Date submitted | 2008 |
| Restricted until | Unrestricted |
| Date published | 2008-10-31 |
| Advisor (committee chair) | Tower, John |
| Advisor (committee member) |
Finkel, Steven E. Aparicio, Oscar Martin Longo, Valter D Comai, Lucio |
| Abstract | The regulation of Drosophila melanogaster longevity and fecundity involves many factors. Longevity is governed by oxidative stress, stem cell loss, dietary restriction, the insulin/IGF-1 pathway, and other factors. Fecundity is also regulated by multiple tissues and factors, including the germline stem cells and stem cell niche, the fat body, yolk proteins, and sex peptides. The fecundity of wild type female Drosophila gradually declines during aging, suggesting a common pathway regulating longevity and fecundity machinery. Since both mechanisms involve multiple factors, sorting through the Gordian’s knot is a formidable task. Using a PdL mutagenesis approach, I screened for a specific phenotype in thousands of independent mutant strains to examine both regulatory networks simultaneously. Two novel genes, magu and hebe, were identified and characterized to regulate longevity and fecundity. While Drosophila lifespan was extended upon the induction of these genes, fecundity increase requires that the gene induction be in an ideal range to show the expected phenotypic change. I also performed several other projects, including studying the lifespan extension effect of dIAP2, characterization of a Drosophila gut driver strain, and intra-abdominal RNAi injection in adult Drosophila. These projects provided us insight on longevity, fecundity, anti-apoptosis, stem cell biology, RNAi and other aspects of Drosophila research. In sum, Drosophila melanogaster, as a model organism for molecular biology and genetics study, will continue to contribute to the scientific community. |
| Keyword | Drosophila; longevity; fecundity |
| Language | English |
| Part of collection | University of Southern California dissertations and theses |
| Publisher (of the original version) | University of Southern California |
| Place of publication (of the original version) | Los Angeles, California |
| Publisher (of the digital version) | University of Southern California. Libraries |
| Provenance | Electronically uploaded by the author |
| Type | texts |
| Legacy record ID | usctheses-m1735 |
| Contributing entity | University of Southern California |
| Rights | Li, Yishi |
| Repository name | Libraries, University of Southern California |
| Repository address | Los Angeles, California |
| Repository email | cisadmin@lib.usc.edu |
| Filename | etd-Li-2382 |
| Archival file | uscthesesreloadpub_Volume44/etd-Li-2382.pdf |
Description
| Title | Page 12 |
| Contributing entity | University of Southern California |
| Repository email | cisadmin@lib.usc.edu |
| Full text | 2 The Drosophila aging process is affected by an array of factors including, but not limited to, oxidative and heat-shock stress responses, insulin/IGF-1 signaling pathway, dietary restriction (DR), and stem cell maintenance. Oxidative stress response has long been known to be involved in the aging process. As respiration occurs, oxygen is metabolized, and reactive oxygen species (ROS) are inevitably released by mitochondria as a by-product. ROS have deleterious effects in most tissues and are generally suppressed by various endogenous enzymes, including superoxide dismutase (SOD) and catalase. Over-expression of these enzymes is sometimes effective to extend Drosophila lifespan (Sun and Tower 1999; Sun, Folk et al. 2002; Sun, Molitor et al. 2004). Heat-shock proteins have also been shown to be beneficial for lifespan extension via increased stress resistance (Morrow, Samson et al. 2004; Wang, Benzer et al. 2004). Among the most investigated heat-shock proteins are Hsp22 and Hsp23, where expression level correlates with life span (Kurapati, Passananti et al. 2000). The Insulin/IGF-1 pathway is conserved among various organisms including C.elegans and Drosophila (Giannakou and Partridge 2007). Functionally conserved components in this pathway include the insulin receptor (InR), phosphoinositide 3-kinase (PI3K) and the forkhead transcription factor dFOXO. When certain critical components in the insulin/IGF-1 pathway are knocked down, such as IGF receptor or the receptor substrate |
