The polo-like protein kinases Fnk and Snk associate with a Ca(2+)- and integrin-binding protein and are regulated dynamically with synaptic plasticity.

In order to stabilize changes in synaptic strength, neurons activate a program of gene expression that results in alterations of their molecular composition and structure. Here we demonstrate that Fnk and Snk, two members of the polo family of cell cycle associated kinases, are co-opted by the brain to serve ...
in this program. Stimuli that produce synaptic plasticity, including those that evoke long-term potentiation (LTP), dramatically increase levels of both kinase mRNAs. Induced Fnk and Snk proteins are targeted to the dendrites of activated neurons, suggesting that they mediate phosphorylation of proteins in this compartment. Moreover, a conserved C-terminal domain in these kinases is shown to interact specifically with Cib, a Ca(2+)- and integrin-binding protein. Together, these studies suggest a novel signal transduction mechanism in the stabilization of long-term synaptic plasticity.
Mesh Terms:
Amino Acid Sequence, Animals, Base Sequence, Calcium-Binding Proteins, Carrier Proteins, Cell Cycle Proteins, DNA Primers, Drosophila Proteins, Hippocampus, Male, Molecular Sequence Data, Nerve Tissue Proteins, Neuronal Plasticity, Protein-Serine-Threonine Kinases, RNA, Messenger, Rats, Rats, Sprague-Dawley, Sequence Homology, Amino Acid, Synapses
EMBO J.
Date: Oct. 15, 1999
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