Journal
NEUROBIOLOGY OF DISEASE
Volume 51, Issue -, Pages 13-26Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2012.01.009
Keywords
Mitochondrial fission; Mitochondrial fusion; Mitochondrial transport; Protein phosphorylation; Dynamin-related protein 1; Mitofusin; Optic atrophy 1; Neurodegeneration; Charcot-Marie-Tooth disease; Autosomal dominant optic atrophy; Synaptic transmission; Synaptogenesis
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Funding
- National Institute of Health [NS043254, NS056244, NS057714]
- National Research Service Award Predoctoral Fellowship [NS077563]
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Nascent evidence indicates that mitochondrial fission, fusion, and transport are subject to intricate regulatory mechanisms that intersect with both well-characterized and emerging signaling pathways. While it is well established that mutations in components of the mitochondrial fission/fusion machinery can cause neurological disorders, relatively little is known about upstream regulators of mitochondrial dynamics and their role in neurodegeneration. Here, we review posttranslational regulation of mitochondrial fission/fusion enzymes, with particular emphasis on dynamin-related protein 1 (Drp1), as well as outer mitochondrial signaling complexes involving protein kinases and phosphatases. We also review recent evidence that mitochondrial dynamics has profound consequences for neuronal development and synaptic transmission and discuss implications for clinical translation. (C) 2012 Elsevier Inc. All rights reserved.
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