Cited by 598Mitochondrial Function and PathologyNeuroscience and Neuropharmacology ResearchAutophagy in Disease and Therapy

Docking of Axonal Mitochondria by Syntaphilin Controls Their Mobility and Affects Short-Term Facilitation

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Kang, Jian-Sheng, Tian, Jin-Hua, Pan, Ping-Yue, Zald, Philip, Li, Cuiling, Deng, Chuxia, Sheng, Zu-Hang·2008·Cell

Abstract

Proper distribution of mitochondria within axons and at synapses is critical for neuronal function. While one-third of axonal mitochondria are mobile, a large proportion remains in a stationary phase. However, the mechanisms controlling mitochondrial docking within axons remain elusive. Here, we report a role for axon-targeted syntaphilin (SNPH) in mitochondrial docking through its interaction with microtubules. Axonal mitochondria that contain exogenously or endogenously expressed SNPH lose mobility. Deletion of the mouse snph gene results in a substantially higher proportion of axonal mitochondria in the mobile state and reduces the density of mitochondria in axons. The snph mutant neurons exhibit enhanced short-term facilitation during prolonged stimulation, probably by affecting calcium signaling at presynaptic boutons. This phenotype is fully rescued by reintroducing the snph gene into the mutant neurons. These findings demonstrate a molecular mechanism for controlling mitochondrial docking in axons that has a physiological impact on synaptic function.

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Crossref · 10.1016/j.cell.2007.11.024

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  • Ca2+ is a key regulator of mitochondria motility and docking.

    “it has been largely described that Ca2+ is a key regulator of mitochondria motility and docking44–49,107.”

    From CYFIP1 governs the development of cortical axons by modulating calcium availability (2025) · cites this paper as [45]

    The Discussion reports that disrupting mitochondrial docking changes presynaptic Ca2+ dynamics—the reverse of the claimed regulatory direction. The Results identify syntaphilin-mediated docking and nerve growth factor signaling as influences on motility, but the searched passages do not say that Ca2+ regulates mitochondrial motility or docking. (LLM, conf=0.76)

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Cited by

Sorted by citations

Authors
Kang, J.-S., Tian, J.-H., Pan, P.-Y., Zald, P., Li, C., Deng, C., & Sheng, Z.-H.
Affiliations
National Institutes of Health (US)
Corresponding author
Sheng, Zu-Hang
Venue
Cell
Publisher
Elsevier BV
Published
2008-01
Volume
132
Issue
1
Pages
137-148
ISSN
0092-8674 (ISSN-L)
OpenAlex
W2112546324
Cited by
598
References
0
Citations by year
2026: 36 · 2025: 27 · 2024: 42 · 2023: 30 · 2022: 38 · 2021: 45 · 2020: 43 · 2019: 45 · 2018: 35 · 2017: 40 · 2016: 36 · 2015: 28 · 2014: 21 · 2013: 34 · 2012: 24
FWCI
9.37
Type
journal article
Language
en
Open access
Locations
  • Cell (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Institute of Neurological Disorders and Stroke (Z01NS002946)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
syntaphilin, axonal mitochondria, microtubules, short-term facilitation, presynaptic terminals, calcium signaling, synaptic function
MeSH terms
Animals, Animals, Newborn, Axons, Axonal Transport, Cells, Cultured, Energy Metabolism, Hippocampus, Membrane Proteins, Microtubule-Associated Proteins, Microtubules, Mitochondria, Mutation, Nerve Tissue Proteins, Rats, Sprague-Dawley, Presynaptic Terminals, Mice, Knockout, Calcium Signaling, Vesicular Transport Proteins, Mice, Rats

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