Mitochondrial trafficking in neurons

TL Schwarz - Cold Spring Harbor perspectives in biology, 2013 - cshperspectives.cshlp.org
TL Schwarz
Cold Spring Harbor perspectives in biology, 2013cshperspectives.cshlp.org
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 …
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.
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