Authors

Susannah Bloom

Senior Project Advisor

Adrienne Wang

Document Type

Project - Campus-only Access

Publication Date

Fall 2024

Keywords

Innate Immunity, Mitochondrial Dysfunction, mtDNA, Imd, Antimicrobial Peptides, Diptericin

Abstract

Age has long been linked to mitochondrial function. As we age, mitochondrial integrity declines, resulting in inefficient respiration, decreased membrane potential and “leakage” of mitochondrial components into the cytoplasm. Aging has also been linked to dysregulation of innate immune signaling, leading to inflammation and a reduction in response to acute infection. More recently, research has implicated mtDNA as a potential upstream signal for innate immune responses, suggesting a link between these two processes thought to drive aging. Preliminary data from the Wang lab has shown that in Drosophila, mtDNA depletion leads to upregulation of the innate immune response. Here, we are validating those findings in a fly that induces mtDNA depletion in a heat-controlled manner, using RT-qPCR to measure expression of Diptericin—an antimicrobial peptide whose expression increases during the fruit fly innate immune response.

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

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