The Mammalian-Specific Protein Armcx1 Regulates Mitochondrial Transport during Axon Regeneration
Autor: | Siwei Li, Thomas Schwarz, Romain Cartoni, Yiling Zhang, Michael W. Norsworthy, Zhigang He, Christopher V. Gabel, Chen Wang, Fengfeng Bei |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Retinal Ganglion Cells medicine.medical_treatment Mitochondrion Biology Retinal ganglion Time-Lapse Imaging Retina Article Mitochondrial Proteins 03 medical and health sciences Mice medicine Animals Regeneration Axon Mitochondrial transport In Situ Hybridization Armadillo Domain Proteins Cerebral Cortex Neurons Gene knockdown Microscopy Confocal Regeneration (biology) General Neuroscience Axotomy Biological Transport Optic Nerve Immunohistochemistry Axons Cell biology Mitochondria Nerve Regeneration Disease Models Animal 030104 developmental biology medicine.anatomical_structure nervous system Gene Knockdown Techniques Optic Nerve Injuries Axoplasmic transport Neuroscience |
Zdroj: | Neuron. 94(3) |
ISSN: | 1097-4199 |
Popis: | Mitochondrial transport is crucial for neuronal and axonal physiology. However, whether and how it impacts neuronal injury responses, such as neuronal survival and axon regeneration, remain largely unknown. In an established mouse model with robust axon regeneration, we show that Armcx1, a mammalian-specific gene encoding a mitochondria-localized protein, is up-regulated after axotomy in this high regeneration condition. Armcx1 overexpression enhances mitochondrial transport in adult retinal ganglion cells (RGCs). Importantly, Armcx1 also promotes both neuronal survival and axon regeneration after injury, and these effects depend on its mitochondrial localization. Furthermore, Armcx1 knockdown undermines both neuronal survival and axon regeneration in the high regenerative capacity model, further supporting a key role of Armcx1 in regulating neuronal injury responses in the adult central nervous system (CNS). Our findings suggest that Armcx1 controls mitochondrial transport during neuronal repair. |
Databáze: | OpenAIRE |
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