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First published online May 23, 2008

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Cortical migration converges on C3G

Cerebral cortex development involves a series of neuronal migrations that are regulated through neuronal cell-surface receptors (integrins) interacting with extracellular matrix (ECM) proteins and neighbouring cells (radial glia). Voss and colleagues now report that C3G, a guanine nucleotide exchange factor that can activate, by GTP exchange, signalling from the Ras-like Rap1, acts downstream of neuronal cell-surface receptors to regulate cortical neuron migration in mice (see p. 2139). In C3G-deficient embryos, they report, the cortical preplate does not split into the marginal zone and subplate because of defects in cortical neuron migration. Consequently, the cortical plate does not form, a phenotype that is common to reelin pathway mutants (reelin is an ECM protein that regulates neuronal migration). The attachment of radial glial cells and neurons to the ECM is also disrupted in C3G-deficient embryos, the researchers report. Thus, C3G is essential for two key processes in cortex development - neuronal migration and radial glial attachment - perhaps because reelin and integrin signalling converge at this Ras signalling molecule.

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

Anne K. Voss, Joanne M. Britto, Mathew P. Dixon, Bilal N. Sheikh, Caitlin Collin, Seong-Seng Tan, and Tim Thomas
Development 2008 135: 2139-2149. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Development Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?