Cited by 771Mitochondrial Function and PathologyMicrotubule and mitosis dynamicsHereditary Neurological Disorders

The axonal transport of mitochondria

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Hollenbeck, Peter J., Saxton, William M.·2005·Journal of Cell Science

Abstract

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.

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Crossref · 10.1242/jcs.02745

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Authors
Hollenbeck, P. J., & Saxton, W. M.
Affiliations
  • Purdue University West Lafayette (US)
  • Indiana University Bloomington (US)
Corresponding author
Hollenbeck, Peter J.
Venue
Journal of Cell Science
Published
2005-12-01
Volume
118
Issue
23
Pages
5411-5419
ISSN
  • 0021-9533 (ISSN-L)
  • 1477-9137
OpenAlex
W4297810568
Cited by
771
References
5
Citations by year
2026: 20 · 2025: 23 · 2024: 20 · 2023: 19 · 2022: 31 · 2021: 38 · 2020: 32 · 2019: 30 · 2018: 27 · 2017: 31 · 2016: 39 · 2015: 32 · 2014: 41 · 2013: 46 · 2012: 74
FWCI
2.95
Type
journal article
Language
en
Open access
Locations
  • Journal of Cell Science (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • HighWire Press Open Archive (submittedVersion)
Funders
  • National Institute of General Medical Sciences (R01GM046295)
  • National Institute of Neurological Disorders and Stroke (R01NS027073)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Hereditary Neurological Disorders
Keywords
mitochondrial transport, axonal transport, organelle transport, kinesin, cytoplasmic dynein, kinesin-1, myosin V, F-actin, microtubules, bidirectional transport, PI3K signaling, John Milton, Miro, axonal degeneration, neuropathy, calcium homeostasis, aerobic metabolism
MeSH terms
Animals, Axonal Transport, Dyneins, Humans, Mitochondria, Models, Biological, Myosins, Signal Transduction, Kinesins

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