Page 82 |
Save page Remove page | Previous | 82 of 150 | Next |
|
small (250x250 max)
medium (500x500 max)
Large (1000x1000 max)
Extra Large
large ( > 500x500)
Full Resolution
All (PDF)
|
This page
All
|
72
Knocking out dIAP1 function results in early embryonic cell death and caspase activity
(Hawkins, Wang et al. 1999; Wang, Hawkins et al. 1999). It was also found that dIAP1
is capable of suppressing cell dealth caused by Drosophila caspase drICE activity
(Kaiser, Vucic et al. 1998). The above discoveries suggest that the Drosophila IAP, like
its human counterpart, family may play important roles in apoptosis and aging
processes.
During a pilot screening for extended lifespan strains in Tower lab fly stocks, my
colleague Gary Landis found that a candidate PdL insertion strain exhibits an unusually
long lifespan. (Figure 15) When I took over this research project, I mapped the location
of the PdL insertion. The sequencing data indicates that the insertion is located 5’
upstream of Drosophila IAP2 gene, a member of Drosophila IAP family. By crossing
this PdL strain with either ubiquitous or tissue-specific driver strains, I was able to over-express
the dIAP2 gene. I hypothesized that when overexpressed, dIAP2 may extend
Drosophila lifespan by inhibiting apoptosis pathways during aging.
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 82 |
| Contributing entity | University of Southern California |
| Repository email | cisadmin@lib.usc.edu |
| Full text | 72 Knocking out dIAP1 function results in early embryonic cell death and caspase activity (Hawkins, Wang et al. 1999; Wang, Hawkins et al. 1999). It was also found that dIAP1 is capable of suppressing cell dealth caused by Drosophila caspase drICE activity (Kaiser, Vucic et al. 1998). The above discoveries suggest that the Drosophila IAP, like its human counterpart, family may play important roles in apoptosis and aging processes. During a pilot screening for extended lifespan strains in Tower lab fly stocks, my colleague Gary Landis found that a candidate PdL insertion strain exhibits an unusually long lifespan. (Figure 15) When I took over this research project, I mapped the location of the PdL insertion. The sequencing data indicates that the insertion is located 5’ upstream of Drosophila IAP2 gene, a member of Drosophila IAP family. By crossing this PdL strain with either ubiquitous or tissue-specific driver strains, I was able to over-express the dIAP2 gene. I hypothesized that when overexpressed, dIAP2 may extend Drosophila lifespan by inhibiting apoptosis pathways during aging. |
