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[Molecular mechanisms of neuronal polarity].

Authors
  • Yoshimura, Takeshi
  • Kawano, Yoji
  • Arimura, Nariko
  • Kawabata, Saeko
  • Kaibuchi, Kozo
Type
Published Article
Journal
Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology
Publication Date
Aug 01, 2005
Volume
25
Issue
4
Pages
169–174
Identifiers
PMID: 16190365
Source
Medline
License
Unknown

Abstract

Neurons are one of the most highly polarized cells known and are comprised of two structurally and functionally distinct parts, an axon and dendrites. The specification of the axon is thought to depend on its length relative to the other minor processes, which are called immature neurites. Elongation of one of immature neurites is necessary for axon specification. We previously showed that collapsin response mediator protein-2 (CRMP-2) is critical for specifying axon/dendrite fate, possibly by promoting neurite elongation via microtubule assembly. Here, we showed that glycogen synthase kinase-3beta (GSK-3beta) phosphorylated CRMP-2 at Thr-514 and inactivated it. The expression of the nonphosphorylated form of CRMP-2 or inhibition of GSK-3beta induced the formation of multiple axons in hippocampal neurons. The expression of constitutively active GSK-3beta impaired neuronal polarization, whereas the nonphosphorylated form of CRMP-2 counteracted the inhibitory effects of GSK-3beta, indicating that GSK-3beta regulates neuronal polarity through the phosphorylation of CRMP-2. We here reviewed the molecular mechanisms of the axon formation.

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