Cited by 132Axon Guidance and Neuronal SignalingNeurogenesis and neuroplasticity mechanismsNerve injury and regeneration

Shootin1 interacts with actin retrograde flow and L1-CAM to promote axon outgrowth

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Shimada, Tadayuki, Toriyama, Michinori, Uemura, Kaori, Kamiguchi, Hiroyuki, Sugiura, Tadao, Watanabe, Naoki, Inagaki, Naoyuki·2008·The Journal of Cell Biology

Abstract

Actin polymerizes near the leading edge of nerve growth cones, and actin filaments show retrograde movement in filopodia and lamellipodia. Linkage between actin filament retrograde flow and cell adhesion molecules (CAMs) in growth cones is thought to be one of the mechanisms for axon outgrowth and guidance. However, the molecular basis for this linkage remains elusive. Here, we show that shootin1 interacts with both actin filament retrograde flow and L1-CAM in axonal growth cones of cultured rat hippocampal neurons, thereby mediating the linkage between them. Impairing this linkage, either by shootin1 RNA interference or disturbing the interaction between shootin1 and actin filament flow, inhibited L1-dependent axon outgrowth, whereas enhancing the linkage by shootin1 overexpression promoted neurite outgrowth. These results strengthen the actin flow-CAM linkage model ("clutch" model) for axon outgrowth and suggest that shootin1 is a key molecule involved in this mechanism.

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Crossref · 10.1083/jcb.200712138

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  • LOF of Nrg causes significant reduction in microtubules at synaptic terminals.

    “LOF of Nrg causes significant reduction in microtubules at synaptic terminals (140,141)”

    From Functional genomic screen and network analysis reveal novel modifiers of tauopathy dissociated from tau phosphorylation (2011) · cites this paper as [141]

    The Results sections provided (page numbers unavailable) examine shootin1 and L1-dependent axon outgrowth in hippocampal neurons, not Nrg loss of function at synaptic terminals. Searches for Nrg/neuroglian and for reduced microtubules at synaptic terminals found no passage addressing the claim. (LLM, conf=0.76)

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Authors
Shimada, T., Toriyama, M., Uemura, K., Kamiguchi, H., Sugiura, T., Watanabe, N., & Inagaki, N.
Affiliations
  • Nara Institute of Science and Technology (JP)
  • 1Division of Signal Transduction
  • RIKEN Center for Brain Science (JP)
  • Kyoto University (JP)
Venue
The Journal of Cell Biology
Published
2008-06-02
Volume
181
Issue
5
Pages
817-829
ISSN
  • 0021-9525 (ISSN-L)
  • 1540-8140
OpenAlex
W1981806649
Cited by
132
References
1
Citations by year
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FWCI
3.17
Type
journal article
Language
en
Open access
Licence
cc-by-nc-sa
Locations
  • The Journal of Cell Biology (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
  • NAIST Digital Library (Nara Institute of Science and Technology) (submittedVersion, cc-by-nc-nd)
  • Institutional Repositories DataBase (IRDB) (submittedVersion, cc-by-nc-nd)
Funders
Japan Society for the Promotion of Science (20016017, 20022029)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Axon Guidance and Neuronal Signaling
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
Keywords
actin retrograde flow, L1CAM, axon growth, growth cones, neurite outgrowth, hippocampal neurons, actin polymerization, axon guidance, adhesion molecules
MeSH terms
Actins, Animals, Axons, Cell Line, Fibroblasts, Gene Expression Regulation, Hippocampus, Humans, Models, Biological, Nerve Tissue Proteins, Cytochalasin D, RNA Interference, Neural Cell Adhesion Molecule L1, Green Fluorescent Proteins, Rats

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