Purdue University
Axonal transport and life cycle of mitochondria in Parkinson's disease model
Abstract
dc:description.abstract<p>In neurons, normal distribution and selective removal of mitochondria are essential for preserving compartmentalized cellular function. Parkin, an E3 ubiquitin ligase associated with familial Parkinson’s disease, has been implicated in mitochondrial dynamics and removal. However, it is not clear how Parkin plays a role in mitochondrial turnover in vivo, and whether the mature neurons possess a compartmentalized Parkin-dependent mitochondrial life cycle. Using the live <em>Drosophila</em> nervous system, here, I investigate the involvement of Parkin in mitochondrial dynamics; organelle distribution, morphology and removal. Parkin deficient animals displayed less number of axonal mitochondria without disturbing organelle motility behaviors, morphology and metabolic state. Instead, loss of Parkin produced tubular and reticular mitochondria specifically in motor neuronal cell body. In addition, unlike in immortalized cells <em>in vitro</em>, Parkin-dependent mitophagy was rarely found in our mature neurons. Thus, my results indicate that mitochondrial morphology is restrictively modulated in the cell body in Parkin-dependent manner, and this further proposes an idea that the organelle supply from the cell body is important for the mitochondrial quality control in mature neurons.</p>
Degree
thesis:*- Name thesis:degree_name
- Doctor of Philosophy (PhD)
- Level thesis:degree_level
- Dissertation
- Discipline thesis:degree_discipline
- Biological Science
- Year
- 2016
Author and committee
dc:creator, dc:contributor.*- Author dc:creator
-
- Sung, Hyun
- Contributors dc:contributor
-
- Peter J. Hollenbeck
- Henry C. Chang
- Jean-Christophe Rochet
- Daniel M. Suter
Subjects
dc:subject × 13Identifiers
dc:identifier.*- Repository record dc:identifier
- https://docs.lib.purdue.edu/open_access_dissertations/714
- OAI identifier oai:identifier
- oai:docs.lib.purdue.edu:open_access_dissertations-1871