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Disruption of mitochondrial DNA replication in Drosophila increases mitochondrial fast axonal transport in vivo

Baqri, Rehan M ; Turner, Brittany A ; Rheuben, Mary B ; Hammond, Bradley D ; Kaguni, Laurie S ; Miller, Kyle E Feany, Mel B.

PloS one, 2009-11, Vol.4 (11), p.e7874-e7874 [Periódico revisado por pares]

United States: Public Library of Science

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Disruption of mitochondrial DNA replication in Drosophila increases mitochondrial fast axonal transport in vivo
Autor: Baqri, Rehan M ; Turner, Brittany A ; Rheuben, Mary B ; Hammond, Bradley D ; Kaguni, Laurie S ; Miller, Kyle E
Feany, Mel B.
Assuntos: Alzheimer's disease ; Alzheimers disease ; Amyotrophic lateral sclerosis ; Animals ; Anterograde transport ; Apoptosis ; Autophagy ; Axonal transport ; Axons - metabolism ; Biochemistry ; Biochemistry/ and Repair ; Biosynthesis ; Caenorhabditis elegans ; Cell Biology/Cellular Death and Stress Responses ; Cell Biology/Cytoskeleton ; Cell Biology/Neuronal and Glial Cell Biology ; Confocal microscopy ; Deoxyribonucleic acid ; Diseases ; Disruption ; DNA ; DNA - chemistry ; DNA biosynthesis ; DNA polymerase ; DNA Replication ; DNA, Mitochondrial - genetics ; DNA-directed DNA polymerase ; Drosophila ; Drosophila - genetics ; Electron microscopy ; Electron transport ; Evolution ; Genetics and Genomics/Animal Genetics ; Green Fluorescent Proteins - chemistry ; Growth factors ; Image Processing, Computer-Assisted ; Immunohistochemistry - methods ; Insects ; Kinesin ; Kinesin - chemistry ; Medicine ; Metabolism ; Microscopy, Confocal - methods ; Microscopy, Electron - methods ; Mitochondria ; Mitochondrial DNA ; Molecular biology ; Movement disorders ; Muscles ; Mutants ; Mutation ; Nematodes ; Nerves ; Neural stem cells ; Neurodegeneration ; Neurodegenerative diseases ; Neuroscience/Neurobiology of Disease and Regeneration ; Neurosciences ; Ophthalmoplegia ; Organic Chemicals - pharmacology ; Oxidative stress ; Parkinson's disease ; Phosphorylation ; Replication ; Science ; Studies ; Transport ; Zoology
É parte de: PloS one, 2009-11, Vol.4 (11), p.e7874-e7874
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
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Conceived and designed the experiments: RMB LK KEM. Performed the experiments: RMB BAT MBR. Analyzed the data: RMB BAT MBR. Contributed reagents/materials/analysis tools: RMB BDH LK KEM. Wrote the paper: RMB MBR LK KEM.
Descrição: Mutations in mitochondrial DNA polymerase (pol gamma) cause several progressive human diseases including Parkinson's disease, Alper's syndrome, and progressive external ophthalmoplegia. At the cellular level, disruption of pol gamma leads to depletion of mtDNA, disrupts the mitochondrial respiratory chain, and increases susceptibility to oxidative stress. Although recent studies have intensified focus on the role of mtDNA in neuronal diseases, the changes that take place in mitochondrial biogenesis and mitochondrial axonal transport when mtDNA replication is disrupted are unknown. Using high-speed confocal microscopy, electron microscopy and biochemical approaches, we report that mutations in pol gamma deplete mtDNA levels and lead to an increase in mitochondrial density in Drosophila proximal nerves and muscles, without a noticeable increase in mitochondrial fragmentation. Furthermore, there is a rise in flux of bidirectional mitochondrial axonal transport, albeit with slower kinesin-based anterograde transport. In contrast, flux of synaptic vesicle precursors was modestly decreased in pol gamma-alpha mutants. Our data indicate that disruption of mtDNA replication does not hinder mitochondrial biogenesis, increases mitochondrial axonal transport, and raises the question of whether high levels of circulating mtDNA-deficient mitochondria are beneficial or deleterious in mtDNA diseases.
Editor: United States: Public Library of Science
Idioma: Inglês

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Disruption of mitochondrial DNA replication in Drosophila increases mitochondrial fast axonal transport in vivo

Baqri, Rehan M ; Turner, Brittany A ; Rheuben, Mary B ; Hammond, Bradley D ; Kaguni, Laurie S ; Miller, Kyle E Feany, Mel B.

United States: Public Library of Science

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