Disruption of Kif5c mediated movement affects mitochondrial form, function and cellular health in rat primary cortical neurons and astrocytes

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(Thesis) M.Sc.
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A clear understanding of mitochondrial dynamics is important in neurodegenerative diseases. Due to the unique architecture of neurons, trafficking of mitochondria throughout processes to regions of high energetic demand is critical to sustain neuronal health. I evaluated the consequences of disrupted kif5c mediated mitochondrial movement on form and function. Morphology and cellular distribution of mitochondria were affected predominantly due to remodelling, which resulted in punctate shaped mitochondria. We also demonstrated that punctate mitochondria resulted in decreased ROS and increased ATP cellular levels. Neurons overexpressing the dominant negative form of kif5c exhibited greater survival than controls following excitotoxicity, suggesting that the kinesin mutant conferred some form of neuroprotection. Our results suggest a novel role of kif5c. In addition to mediating mitochondrial transport, kif5c plays a role in the mechanism of regulating mitochondrial morphology. Our results suggest that kif5c mediated mitochondrial dynamics may play an important role in regulating various mitochondrial functions and in turn cellular health.
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Thesis advisor: Rintoul, Gordon
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