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Focal adhesion kinase modulates radial glia-dependent neuronal migration through Connexin-26

AuthorsValiente, Manuel; Ciceri, Gabriele; Rico, Beatriz; Marín Parra, Óscar
Issue Date2011
PublisherSociety for Neuroscience
CitationJournal of Neuroscience 31(32): 11678-11691 (2011)
AbstractFocal adhesion kinase (FAK) is an intracellular kinase and scaffold protein that regulates migration in many different cellular contexts but whose function in neuronal migration remains controversial. Here, we have analyzed the function of FAK in two populations of neurons with very distinct migratory behaviors: cortical interneurons, which migrate tangentially and independently of radial glia; and pyramidal cells, which undergo glial-dependent migration. We found that FAK is dispensable for glial-independent migration but is cell-autonomously required for the normal interaction of pyramidal cells with radial glial fibers. Loss ofFAKfunction disrupts the normal morphology of migrating pyramidal cells, delays migration, and increases the tangential dispersion of neurons arising from the same radial unit.FAKmediates this process by regulating the assembly of Connexin-26 contact points in the membrane of migrating pyramidal cells. These results indicate that FAK plays a fundamental role in the dynamic regulation of Gap-mediated adhesions during glial-guided neuronal migration in the mouse. © 2011 the authors.
Identifiersdoi: 10.1523/JNEUROSCI.2678-11.2011
issn: 0270-6474
e-issn: 1529-2401
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