The Mammalian-Specific Protein Armcx1 Regulates Mitochondrial Transport during Axon Regeneration.

Published

Journal Article

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 upregulated 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.

Full Text

Duke Authors

Cited Authors

  • Cartoni, R; Norsworthy, MW; Bei, F; Wang, C; Li, S; Zhang, Y; Gabel, CV; Schwarz, TL; He, Z

Published Date

  • December 21, 2016

Published In

Volume / Issue

  • 92 / 6

Start / End Page

  • 1294 - 1307

PubMed ID

  • 28009275

Pubmed Central ID

  • 28009275

Electronic International Standard Serial Number (EISSN)

  • 1097-4199

Digital Object Identifier (DOI)

  • 10.1016/j.neuron.2016.10.060

Language

  • eng

Conference Location

  • United States