Axonal transport and life cycle of mitochondria in Parkinson's disease model
Abstract
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 Drosophila 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 in vitro, 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.
Degree
Ph.D.
Advisors
Hollenbeck, Purdue University.
Subject Area
Molecular biology|Neurosciences|Genetics|Cellular biology|Biochemistry
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