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Neuronal migration is critical for establishing neocortical cell layers and migration defects can cause neurological and psychiatric diseases. Recent studies show that radially migrating neocortical neurons use glia-dependent and glia-independent modes of migration, but the signaling pathways that control different migration modes and the transitions between them are poorly defined. Here, we show that Dab1, an essential component of the reelin pathway, is required in radially migrating neurons for glia-independent somal translocation, but not for glia-guided locomotion. During migration, Dab1 acts in translocating neurons to stabilize their leading processes in a Rap1-dependent manner. Rap1, in turn, controls cadherin function to regulate somal translocation. Furthermore, cell-autonomous neuronal deficits in somal translocation are sufficient to cause severe neocortical lamination defects. Thus, we define the cellular mechanism of reelin function during radial migration, elucidate the molecular pathway downstream of Dab1 during somal translocation, and establish the importance of glia-independent motility in neocortical development.

Original publication

DOI

10.1016/j.neuron.2011.01.003

Type

Journal article

Journal

Neuron

Publication Date

10/02/2011

Volume

69

Pages

482 - 497

Keywords

Animals, Basement Membrane, Cadherins, Cell Adhesion Molecules, Neuronal, Cell Movement, Extracellular Matrix Proteins, Female, Gene Knock-In Techniques, Mice, Mice, Knockout, Mice, Neurologic Mutants, Mice, Transgenic, Neocortex, Nerve Tissue Proteins, Neurons, Serine Endopeptidases, rap1 GTP-Binding Proteins