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Journal of Cell Science
Article . 2008 . Peer-reviewed
Data sources: Crossref
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Reduction of Crk and CrkL expression blocks reelin-induced dendritogenesis

Authors: Tohru, Matsuki; Albéna, Pramatarova; Brian W, Howell;

Reduction of Crk and CrkL expression blocks reelin-induced dendritogenesis

Abstract

The reelin signaling pathway regulates nervous system function after birth, in addition to its role in regulating neuronal positioning during embryogenesis. The receptor-dependent, reelin-induced tyrosine phosphorylation of the Dab1 docking protein is an established prerequisite for biological responses to this ligand. Here we show that the inactivation of a conditional Dab1 allele reduces process complexity in correctly positioned neurons in the CA1 region of the mouse hippocampus after birth. Reelin stimulation of cultured hippocampal neurons enhances dendritogenesis by approximately twofold and in a manner dependent on Src family kinases. This enhancement is blocked by reducing expression of Crk family proteins, adaptor molecules that interact with Dab1 in a tyrosine phosphorylation-dependent manner. Retrovirally expressed inhibitory RNAs used to reduce Crk and CrkL expression did not block BDNF-enhanced dendritogenesis or influence axonogenesis. Together, this demonstrates that the Crk family proteins are important downstream components of the reelin signaling pathway in the regulation of postnatal hippocampal dendritogenesis.

Keywords

Mice, Knockout, Extracellular Matrix Proteins, Cell Adhesion Molecules, Neuronal, Pyramidal Cells, Serine Endopeptidases, Down-Regulation, Nuclear Proteins, Cell Differentiation, Nerve Tissue Proteins, Dendrites, Proto-Oncogene Proteins c-crk, Hippocampus, Mice, Reelin Protein, Animals, Phosphorylation, RNA, Small Interfering, Cell Shape, Cells, Cultured, Adaptor Proteins, Signal Transducing

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    citations
    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    80
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 10%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Top 10%
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 10%
Powered by OpenAIRE graph
citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
80
Top 10%
Top 10%
Top 10%
bronze