Journal
NEURON
Volume 40, Issue 3, Pages 501-514Publisher
CELL PRESS
DOI: 10.1016/S0896-6273(03)00666-4
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Funding
- NEI NIH HHS [R01 EY10688] Funding Source: Medline
- NINDS NIH HHS [R01 NS11033, R01 NS19090, F32 NS011033, R01 NS019090-25, R01 NS019090] Funding Source: Medline
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Targeted deletion of focal adhesion kinase (fak) in the developing dorsal forebrain resulted in local disruptions of the cortical basement membrane located between the neuroepithelium and pia-meninges. At disruption sites, clusters of neurons invaded the marginal zone. Retraction of radial glial endfeet, midline fusion of brain hemispheres, and gliosis also occurred, similar to type II cobblestone lissencephaly as seen in congenital muscular dystrophy. Interestingly, targeted deletion of fak in neurons alone did not result in cortical ectopias, indicating that fak deletion from glia is required for neuronal mislocalization. Unexpectedly, fak deletion specifically from meningeal fibroblasts elicited similar cortical ectopias in vivo and altered laminin organization in vitro. These observations provide compelling evidence that FAK plays a key signaling role in cortical basement membrane assembly and/or remodeling. In addition, FAK is required within neurons during development because neuron-specific fak deletion alters dendritic morphology in the absence of lamination defects.
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