The axonal transport of mitochondria
Open accessAbstract
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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Overexpression of Tau WT, 3A, or 3D reduced anterograde movement of mitochondria in PC12 cells and cortical neurons.
“Overexpression of either Tau WT, 3A, or 3D reduced anterograde movement of mitochondria in PC12 cells and cortical neurons, as reported (Mandelkow et al., 2004;Hollenbeck and Saxton, 2005;Dixit et al., 2008).”
From Regulation of Mitochondrial Transport and Inter-Microtubule Spacing by Tau Phosphorylation at the Sites Hyperphosphorylated in Alzheimer's Disease (2012) · cites this paper as Hollenbeck and Saxton, 2005
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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.
- ORCID
- Hollenbeck, Peter J.
- Venue
- Journal of Cell Science
- Publisher
- The Company of Biologists
- 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
- green
- europepmc.org
- 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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