Authors

Lola Demurger

Senior Project Advisor

Adrienne Wang

Document Type

Project

Publication Date

Summer 2022

Keywords

mitochondrial dysfunction, aging, UL12.5, Drosophila, nuclease, mtDNA

Abstract

Mitochondria have long been studied in relation to aging as they are critical to cell operation, and their dysfunction is linked to several age-related factors, such as shortened lifespan and increased innate immunity. In this study, we use a mitochondrially targeted nuclease called UL12.5 to artificially induce mitochondrial dysfunction by degrading the mitochondrial genome in Drosophila. Degraded mitochondrial DNA (mtDNA) has many downstream effects, including mtDNA depletion, mtDNA leakage into the cytoplasm, chronically upregulated innate immune response, and shortened lifespan. We began the process of developing an assay that measured mtDNA depletion as a result of UL12.5-mediated mtDNA degradation in Drosophila. We used qPCR to quantify levels of mtDNA to see if UL12.5 expression was correlated with decreased mtDNA content. Due to low efficiency of the qPCR, continued optimization of the assay is necessary, and this will help our lab validate projects investigating the further downstream effects of UL12.5 expression on age-related factors.

Department

Biology

Type

Text

Rights

Copying of this document in whole or in part is allowable only for scholarly purposes. It is understood, however, that any copying or publication of this document for commercial purposes, or for financial gain, shall not be allowed without the author’s written permission.

Language

English

Format

application/pdf

Included in

Biology Commons

Share

COinS