2009 Fiscal Year Final Research Report
Molecular mechanisms for recognition of neuronal polarity by kinesin
| Project/Area Number |
20700310
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neuroscience in general
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
KONISHI Yoshiyuki Hamamatsu University School of Medicine, 分子イメージング先端研究センター, 准教授 (00382838)
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| Project Period (FY) |
2008 – 2009
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| Keywords | キネシン / トラフィッキング / 微小管 / チュブリン / 神経細胞 |
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| Research Abstract |
Neurons form distinctive axonal and dendritic compartments that are important for directional signaling, but the mechanisms that discriminate axons from dendrites remain elusive. In this study, we found that tyrosinated tubulins that are abundant in somatodendrites prevent kinesin-1 from binding to microtubules, thereby regulate polarized kinesin-1 trafficking to the axon. Consistently, inhibition of tubulin tyrosination in hippocampal neurons disrupted neuronal polarity. Our study identifies a molecular mechanism that discriminates the axonal microtubules from somatodendritic microtubules, and provided novel molecular mechanisms involved in the neuronal morphogenesis.
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[Journal Article] Transmembrane and ubiquitin-like domain-containing protein 1 (Tmub1/HOPS) facilitates surface expression of GluR2-containing AMPA receptors.2008
Author(s)
Yang H, Takagi H, Konishi Y, Ageta H, Ikegami K, Yao I, Sato S, Hatanaka K, Inokuchi K, Seog DH, Setou M
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Journal Title
Peer Reviewed
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