Abstract
Precisely regulated radial migration out of the ventricular zone is essential for corticogenesis. Here, we identify a mechanism that can tether ventricular zone cells in situ. FILIP interacts with Filamin A, an indispensable actin-binding protein that is required for cell motility, and induces its degradation in COS-7 cells. Degradation of Filamin A is identified in the cortical ventricular zone, where filip mRNA is localized. Furthermore, most ventricular zone cells that overexpress FILIP fail to migrate in explants. These results demonstrate that FILIP functions through a Filamin A F-actin axis to control the start of neocortical cell migration from the ventricular zone.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Actins / physiology
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Amino Acid Sequence
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Animals
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COS Cells
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Carrier Proteins / genetics
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Carrier Proteins / physiology*
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Cell Movement
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Contractile Proteins / genetics
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Contractile Proteins / physiology*
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Cytoskeletal Proteins / genetics
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Cytoskeletal Proteins / physiology*
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Cytoskeleton / metabolism
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Filamins
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In Situ Hybridization
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Microfilament Proteins / genetics
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Microfilament Proteins / physiology*
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Molecular Sequence Data
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Neocortex / cytology
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Neocortex / growth & development*
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Rats
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Rats, Wistar
Substances
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Actins
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Carrier Proteins
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Contractile Proteins
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Cytoskeletal Proteins
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FILIP1 protein, human
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Filamins
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Microfilament Proteins