Regulation of spine development by semaphorin3A through cyclin-dependent kinase 5 phosphorylation of collapsin response mediator protein 1

Naoya Yamashita, Asa Morita, Yutaka Uchida, Fumio Nakamura, Hiroshi Usui, Toshio Ohshima, Masahiko Taniguchi, Jérôme Honnorat, Nicole Thomasset, Kohtaro Takei, Takuya Takahashi, Pappachan Kolattukudy, Yoshio Goshima*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

97 Citations (Scopus)

Abstract

Collapsin response mediator protein 1 (CRMP1) is one of the CRMP family members that mediates signal transduction of axonal guidance and neuronal migration. We show here evidence that CRMP1 is involved in semaphorin3A (Sema3A)-induced spine development in the cerebral cortex. In the cultured cortical neurons from crmp1+/- mice, Sema3A increased the density of clusters of synapsin I and postsynaptic density-95, but this increase was markedly attenuated in crmp1-/- mice. This attenuation was also seen in cyclin-dependent kinase 5 (cdk5)-/- neurons. Furthermore, the introduction of wild-type CRMP1 but not CRMP1-T509A/S522A, (Thr 509 and Ser 522 were replaced by Ala), a mutant that cannot be phosphorylated by Cdk5, into crmp1-/- neurons rescued the defect in Sema3A responsiveness. The Golgi-impregnation method showed that the crmp1-/- layer V cortical neurons showed a lower density of synaptic bouton-like structures and that this phenotype had genetic interaction with sema3A. These findings suggest that Sema3A-induced spine development is regulated by phosphorylation of CRMP1 by Cdk5.

Original languageEnglish
Pages (from-to)12546-12554
Number of pages9
JournalJournal of Neuroscience
Volume27
Issue number46
DOIs
Publication statusPublished - 2007 Nov 14

Keywords

  • CRMP
  • Cdk5
  • Cerebral cortex
  • PSD-95
  • Sema3A
  • Spine
  • Synapsin I

ASJC Scopus subject areas

  • Neuroscience(all)

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