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Cold Spring Harb Perspect Biol. 2013 Jun 1;5(6). pii: a011304. doi: 10.1101/cshperspect.a011304.

Mitochondrial trafficking in neurons.

Author information

1
F.M. Kirby Neurobiology Center, Children's Hospital Boston, and Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA. Thomas.schwarz@childrens.harvard.edu

Abstract

Neurons, perhaps more than any other cell type, depend on mitochondrial trafficking for their survival. Recent studies have elucidated a motor/adaptor complex on the mitochondrial surface that is shared between neurons and other animal cells. In addition to kinesin and dynein, this complex contains the proteins Miro (also called RhoT1/2) and milton (also called TRAK1/2) and is responsible for much, although not necessarily all, mitochondrial movement. Elucidation of the complex has permitted inroads for understanding how this movement is regulated by a variety of intracellular signals, although many mysteries remain. Regulating mitochondrial movement can match energy demand to energy supply throughout the extraordinary architecture of these cells and can control the clearance and replenishing of mitochondria in the periphery. Because the extended axons of neurons contain uniformly polarized microtubules, they have been useful for studying mitochondrial motility in conjunction with biochemical assays in many cell types.

PMID:
23732472
PMCID:
PMC3660831
DOI:
10.1101/cshperspect.a011304
[Indexed for MEDLINE]
Free PMC Article

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