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First published online November 23, 2005
doi: 10.1242/10.1242/jcs.02745
Commentary |
1 Department of Biological Sciences, Purdue University, 915 West State Street, West Lafayette, IN 47907, USA
2 Department of Biology, Indiana University, 1001 East 3rd Street, Bloomington, IN 47405, USA
* Author for correspondence (e-mail: phollenb{at}purdue.edu)
Accepted 17 October 2005
Organelle transport is vital for the development and maintenance of axons, in which the distances between sites of organelle biogenesis, function, and recycling or degradation can be vast. Movement of mitochondria in axons can serve as a general model for how all organelles move: mitochondria are easy to identify, they move along both microtubule and actin tracks, they pause and change direction, and their transport is modulated in response to physiological signals. However, they can be distinguished from other axonal organelles by the complexity of their movement and their unique functions in aerobic metabolism, calcium homeostasis and cell death. Mitochondria are thus of special interest in relating defects in axonal transport to neuropathies and degenerative diseases of the nervous system. Studies of mitochondrial transport in axons are beginning to illuminate fundamental aspects of the distribution mechanism. They use motors of one or more kinesin families, along with cytoplasmic dynein, to translocate along microtubules, and bidirectional movement may be coordinated through interaction between dynein and kinesin-1. Translocation along actin filaments is probably driven by myosin V, but the protein(s) that mediate docking with actin filaments remain unknown. Signaling through the PI 3-kinase pathway has been implicated in regulation of mitochondrial movement and docking in the axon, and additional mitochondrial linker and regulatory proteins, such as Milton and Miro, have recently been described.
Key words: Mitochondria, Axonal transport, Kinesin, Myosin, Dynein
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