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83
Discussion
The first two rounds of experiments showed somewhat contradicting results. In the first
round, although only male flies were assayed for lifespan, almost all the crosses
suggested lifespan extension. On the other hand, in the second round lifespan assays, the
male group lifespan assay was essentially the repeat of the first round, but all the
lifespan extension effects were diminished except the Dy42 motor neuron driver cross.
The best lifespan extension in the first round, given by the Tubulin driver, turned into a
negative effect in the second round. In the female group, lifespan extension was only
observed in Tubulin driver cross, but not any other group. These contradicting results
were especially difficult to analyze because of the lack of wild type control groups. But
by taking a closer look at the comparison between the two rounds of experiments, some
general trends can still be elucidated. The lifespan extension effects in the second round
were generally diminished relative to the first round. The extension from Dy42 in the
second round was obviously less than in the first round. Rather than the positive effect
that was shown in the first round, the Tubulin cross resulted in a negative effect in the
second round. Although we cannot be certain, the overall decaying trend could be due to
a decreased expression of rtTA transcription activator across all the driver lines. Because
DOX is a light-sensitive reagent, leaving the DOX stock solution in room temperature or
exposing it to strong sunlight for an extended period of time could result in the
degradation of the reagent. A degraded DOX stock solution could lower the efficiency
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 93 |
| Contributing entity | University of Southern California |
| Repository email | cisadmin@lib.usc.edu |
| Full text | 83 Discussion The first two rounds of experiments showed somewhat contradicting results. In the first round, although only male flies were assayed for lifespan, almost all the crosses suggested lifespan extension. On the other hand, in the second round lifespan assays, the male group lifespan assay was essentially the repeat of the first round, but all the lifespan extension effects were diminished except the Dy42 motor neuron driver cross. The best lifespan extension in the first round, given by the Tubulin driver, turned into a negative effect in the second round. In the female group, lifespan extension was only observed in Tubulin driver cross, but not any other group. These contradicting results were especially difficult to analyze because of the lack of wild type control groups. But by taking a closer look at the comparison between the two rounds of experiments, some general trends can still be elucidated. The lifespan extension effects in the second round were generally diminished relative to the first round. The extension from Dy42 in the second round was obviously less than in the first round. Rather than the positive effect that was shown in the first round, the Tubulin cross resulted in a negative effect in the second round. Although we cannot be certain, the overall decaying trend could be due to a decreased expression of rtTA transcription activator across all the driver lines. Because DOX is a light-sensitive reagent, leaving the DOX stock solution in room temperature or exposing it to strong sunlight for an extended period of time could result in the degradation of the reagent. A degraded DOX stock solution could lower the efficiency |
