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

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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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