The polo-like protein kinases Fnk and Snk associate with a Ca2+- and integrin-binding protein and are regulated dynamically with synaptic plasticity

In order to stabilize changes in synaptic strength, neurons activate a prog ram of gene expression that results in alterations of their molecular compo sition 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, includ ing those that evoke long-term, potentiation (LTP), dramatically increase l evels of both kinase mRNAs. Induced Fnk and Snk proteins are targeted to th e dendrites of activated neurons, suggesting that they mediate phosphorylat ion of proteins in this compartment. Moreover, a conserved C-terminal domai n in these kinases is shown to interact specifically with Cib, a Ca2+- and integrin-binding protein, Together, these studies suggest a novel signal tr ansduction mechanism in the stabilization of long-term synaptic plasticity.