Title

Regulation of spine development by Semaphorin3A through cyclin-dependent kinase 5 phosphorylation of collapsin response mediator protein 1

Authors

Authors

N. Yamashita; A. Morita; Y. Uchida; F. Nakamura; H. Usui; T. Ohshima; M. Taniguchi; J. Honnorat; N. Thomasset; K. Takei; T. Takahashi; P. Kolattukudy;Y. Goshima

Comments

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Abbreviated Journal Title

J. Neurosci.

Keywords

CRMP; Sema3A; Cdk5; spine; PSD-95; synapsin I; cerebral cortex; GROWTH CONE COLLAPSE; AXON GUIDANCE; RAT-BRAIN; CDK5; CRMP-2; FAMILY; RECEPTORS; MORPHOGENESIS; ENDOCYTOSIS; EXPRESSION; Neurosciences

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.

Journal Title

Journal of Neuroscience

Volume

27

Issue/Number

46

Publication Date

1-1-2007

Document Type

Article

Language

English

First Page

12546

Last Page

12554

WOS Identifier

WOS:000250952700014

ISSN

0270-6474

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