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30
and rtTA(3)E2 can cause robust over-expression of a gene located 3’ to PdL in all of the
somatic tissues of the fly.
Figure 4: The first fecundity test after balancing to homozygosity. Male flies from each
strain was crossed to rtTA(3)E2 virgin females. The progeny females were kept with
young Or-R males for continued mating. The fecundity was assayed with the method
described in methods section. X-axis represents the early and late time period. Y-axis
represents progeny per female per day. Y-error bar represents standard deviation. A t-test
comparing the early and late time period fecundity was performed, and the p-value
is shown under each curve.
Strain PdL[45C1] contains an insert of PdL on the second chromosome, which is also
marked with the dominant mutation Sternopleural (Sp). Virgins of this strain were
crossed to males from strain delta2-3, which expresses the P element transposase. The
male progeny containing both the PdL[45C1] insertion and delta2-3 were selected by
their phenotypic markers. In these males the transposase will cause transposition of PdL
to new sites in the genome in the germ line cells, and therefore these males are called
“dysgenic”. The dysgenic males were crossed to virgins of strain rtTA(3)E2 to produce
mutant female progeny bearing a new insertion of PdL on either the first, second or third
chromosomes (indicated by asterisk), as well as the rtTA(3)E2 driver. The new
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 40 |
| Contributing entity | University of Southern California |
| Repository email | cisadmin@lib.usc.edu |
| Full text | 30 and rtTA(3)E2 can cause robust over-expression of a gene located 3’ to PdL in all of the somatic tissues of the fly. Figure 4: The first fecundity test after balancing to homozygosity. Male flies from each strain was crossed to rtTA(3)E2 virgin females. The progeny females were kept with young Or-R males for continued mating. The fecundity was assayed with the method described in methods section. X-axis represents the early and late time period. Y-axis represents progeny per female per day. Y-error bar represents standard deviation. A t-test comparing the early and late time period fecundity was performed, and the p-value is shown under each curve. Strain PdL[45C1] contains an insert of PdL on the second chromosome, which is also marked with the dominant mutation Sternopleural (Sp). Virgins of this strain were crossed to males from strain delta2-3, which expresses the P element transposase. The male progeny containing both the PdL[45C1] insertion and delta2-3 were selected by their phenotypic markers. In these males the transposase will cause transposition of PdL to new sites in the genome in the germ line cells, and therefore these males are called “dysgenic”. The dysgenic males were crossed to virgins of strain rtTA(3)E2 to produce mutant female progeny bearing a new insertion of PdL on either the first, second or third chromosomes (indicated by asterisk), as well as the rtTA(3)E2 driver. The new |
