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CNS neuronal focal adhesion kinase forms clusters that co‐localize with vinculin
Author(s) -
Stevens Gerin R.,
Zhang Chi,
Berg Margaret M.,
Lambert Mary P.,
Barber Kirsten,
Cantallops Isabel,
Routtenberg Aryeh,
Klein William L.
Publication year - 1996
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19961115)46:4<445::aid-jnr6>3.0.co;2-g
Subject(s) - focal adhesion , vinculin , microbiology and biotechnology , biology , neurite , integrin , actin cytoskeleton , ptk2 , growth cone , signal transduction , fibronectin , extracellular matrix , neural cell adhesion molecule , cytoskeleton , axon , cell adhesion , receptor , cell , protein kinase c , biochemistry , mitogen activated protein kinase kinase , in vitro
Focal adhesion kinase (FAK) is a non‐receptor protein tyrosine kinase that appears to play a central role in integrin‐mediated signal transduction in non‐neuronal cells, linking the extracellular matrix to the actin‐based cytoskeleton at focal adhesion contacts. Biochemical analysis has revealed the presence of FAK immunoreactivity in cells of neuronal lineage (Zhang et al., 1994) and in the CNS (Burgaya et al. 1995; Grant et al., 1995). In the current work, we have examined the immunodistribution of FAK in nerve cell cultures and tissue sections from the rat CNS. Cultures of B103 CNS neuroblastoma cells and primary cultures of hippocampal neurons both showed abundant FAK immunoreactivity in nerve cell bodies. Immunoreactivity also extended into neurites and growth cones. The most striking feature of FAK distribution was the presence of short, punctate clusters of high FAK concentration. These FAK clusters were maintained in triton‐extracted cell ghosts, indicating association with the cytoskeleton. Double‐label confocal imaging showed that clusters of FAK coincided with clusters of vinculin, another actin‐associated signal transduction molecule implicated in control of growth cone motility. Data from hippocampal sections verified the presence of FAK in adult neurons where it was enriched in somato‐dendritic domains and showed a non‐uniform distribution. Quantitative FAK immunoprecipitation to compare adult with embryonic brain showed a 7‐fold developmental down‐regulation of FAK and a 21‐fold down‐regulation of FAK TyrP. The data suggest that neuronal FAK may participate in signal transduction complexes relevant to neuronal morphogenesis and plasticity. © 1996 Wiley‐Liss, Inc.