C3G regulates cortical neuron migration, preplate splitting and radial glial cell attachment

Voss, Anne K., Britto, Joanne M., Dixon, Mathew P., Sheikh, Bilal N., Collin, Caitlin, Tan, Seong-Seng and Thomas, Tim (2008) C3G regulates cortical neuron migration, preplate splitting and radial glial cell attachment. Development, 135 12: 2139-2149. doi:10.1242/dev.016725

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Author Voss, Anne K.
Britto, Joanne M.
Dixon, Mathew P.
Sheikh, Bilal N.
Collin, Caitlin
Tan, Seong-Seng
Thomas, Tim
Title C3G regulates cortical neuron migration, preplate splitting and radial glial cell attachment
Journal name Development   Check publisher's open access policy
ISSN 0950-1991
1477-9129
Publication date 2008-01-01
Year available 2008
Sub-type Article (original research)
DOI 10.1242/dev.016725
Open Access Status File (Publisher version)
Volume 135
Issue 12
Start page 2139
End page 2149
Total pages 11
Place of publication Cambridge, United Kingdom
Publisher The Company of Biologists Ltd.
Language eng
Subject 1307 Cell Biology
2702 Anatomy
Formatted abstract
Neuronal migration is integral to the development of the cerebral cortex and higher brain function. Cortical neuron migration defects lead to mental disorders such as lissencephaly and epilepsy. Interaction of neurons with their extracellular environment regulates cortical neuron migration through cell surface receptors. However, it is unclear how the signals from extracellular matrix proteins are transduced intracellularly. We report here that mouse embryos lacking the Ras family guanine nucleotide exchange factor, C3G (Rapgef1, Grf2), exhibit a cortical neuron migration defect resulting in a failure to split the preplate into marginal zone and subplate and a failure to form a cortical plate. C3G-deficient cortical neurons fail to migrate. Instead, they arrest in a multipolar state and accumulate below the preplate. The basement membrane is disrupted and radial glial processes are disorganised and lack attachment in C3G-deficient brains. C3G is activated in response to reelin in cortical neurons, which, in turn, leads to activation of the small GTPase Rap1. In C3G-deficient cells, Rap1 GTP loading in response to reelin stimulation is reduced. In conclusion, the Ras family regulator C3G is essential for two aspects of cortex development, namely radial glial attachment and neuronal migration.
Keyword Cell adhesion
Cerebral cortex
Mouse
Neuronal migration
Radial glia
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: Queensland Brain Institute Publications
 
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Created: Tue, 28 Oct 2014, 03:18:19 EST by Sylvie Pichelin on behalf of Queensland Brain Institute