Human mtDNA Copy Number Quantification
Abstract
Our social worlds and physical health are profoundly intertwined, but we have limited tools for studying these important connections. Within the recent psychiatric literature, changes in mitochondrial DNA copy number (mtDNAcn) have been linked to a variety of socially influenced mental illnesses such as major depression. In principle, this biomarker may therefore also be responsive to more subtle changes in our social environments, including life events that attenuate stress.
This poster outlines plans for a novel molecular study of how interspecies social bonding impacts human cells. Specifically, we propose to use quantitative PCR to measure the abundances of (single copy) mitochondrial genes alongside (single copy) nuclear control loci over the course of social bond development in humans adopting shelter animals. This approach will reveal whether mitochondrial DNA levels are modulated when the focal humans instantiate a 15,000-year-old co-evolved mutualism with domesticated dogs. While other outcomes are possible, we predict on the basis of recent psychiatric studies that bonding will result in declining stress, mtDNA concentrations, and mtDNA polymorphism (aka “heteroplasmy”).
Faculty Sponsors
Dr. Eben Gering
Project Type
Event
Location
Alvin Sherman Library
Start Date
4-6-2022 12:00 PM
End Date
4-7-2022 5:00 PM
Human mtDNA Copy Number Quantification
Alvin Sherman Library
Our social worlds and physical health are profoundly intertwined, but we have limited tools for studying these important connections. Within the recent psychiatric literature, changes in mitochondrial DNA copy number (mtDNAcn) have been linked to a variety of socially influenced mental illnesses such as major depression. In principle, this biomarker may therefore also be responsive to more subtle changes in our social environments, including life events that attenuate stress.
This poster outlines plans for a novel molecular study of how interspecies social bonding impacts human cells. Specifically, we propose to use quantitative PCR to measure the abundances of (single copy) mitochondrial genes alongside (single copy) nuclear control loci over the course of social bond development in humans adopting shelter animals. This approach will reveal whether mitochondrial DNA levels are modulated when the focal humans instantiate a 15,000-year-old co-evolved mutualism with domesticated dogs. While other outcomes are possible, we predict on the basis of recent psychiatric studies that bonding will result in declining stress, mtDNA concentrations, and mtDNA polymorphism (aka “heteroplasmy”).
