Date of Award
Spring 5-15-2016
Degree Name
Doctor of Philosophy (PhD)
Degree Type
Dissertation
Abstract
Mitochondria are essential for neuronal function; they provide energy (ATP) to maintain ionic gradients and support synaptic function, and participate in Ca2+ buffering. The complex morphology of neurons presents a unique challenge for mitochondria. Axons and dendrites are long and highly branched, and mitochondria must traffic from the soma and distribute throughout these projections to reach sites of demand. In dendrites, stationary mitochondria localize to sites of high energy consumption and Ca2+ signaling, including synapses and branch points. To understand how these distribution patterns arise during dendritic development, we analyzed the trafficking of mitochondria in dendrites of ganglion cells (GCs) in the intact developing mouse retina. Genetic mutations that disrupt mitochondrial distribution through dendritic branches underlie many common neuropathies, including Dominant Optic Atrophy (DOA). Understanding the mechanisms and functional significance of mitochondrial distribution in neurons is essential for the understanding and treatment of these diseases. We examined mitochondrial distribution and function in a mouse model of DOA to understand how mitochondrial defects give rise to neural pathologies.
Language
English (en)
Chair and Committee
Daniel Kerschensteiner
Committee Members
James Skeath, Aaron Diantonio, Kelly Monk, Valeria Cavalli,
Recommended Citation
Faits, Michelle, "Mitochondrial Transport and Function in Development and Disease" (2016). Arts & Sciences Electronic Theses and Dissertations. 728.
https://openscholarship.wustl.edu/art_sci_etds/728
Included in
Cell Biology Commons, Developmental Biology Commons, Neuroscience and Neurobiology Commons
Comments
Permanent URL: https://doi.org/10.7936/K7G15Z46