Published online 28 June 2004. doi:10.1083/jcb1661iti4
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 166, Number 1, 7-7
Myelin movement
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Transport fails when oligodendrocytes are defective.
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Like the hard candy shell around an M&M, oligodendrocytes swathe axons with a sheath of myelin for protection. Now, Edgar et al. (page 121) show that the myelin casing may do more than just provide shelter and stability; it may also set up conditions necessary for fast axonal transport.
The team noticed multiple organelles amassed within optic nerve axons in mice with a null mutation of the Plp gene, which encodes two major proteins of the myelin sheath. These organelle traffic jams implied that there might be problems with transport in these cells. So Edgar et al. looked at movement of labeled tracers in fast anterograde and retrograde transport. There were minor defects in fast forward transport that took some time to accumulate, and severe defects in fast backward transport. A closer look at motor proteins revealed that levels of the retrograde motor dynein and associated dynactin were elevated, possibly due to the accumulation of proteins on stalled vesicles. Anterograde motors were unaffected.
The primary function of myelin is to insulate nerves and thus speed transduction of nerve impulses. But it has also been shown to affect mitochondrial placement and cytoskeleton function in the underlying neuron. Exactly how the oligodendrocyte is communicating with the neuron to achieve such tasks, and which of these events are necessary for fast axonal transport, remains uncertain. 
Aparna Sreenivasan
aparnas{at}nasw.org
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