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| The EMBO Journal
(1999) 18, 5528–5539, doi:10.1093/emboj/18.20.5528 |
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| The polo-like protein kinases Fnk and Snk associate with a Ca2+- and integrin-binding protein and are regulated dynamically with synaptic plasticity |
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| Gunther Kauselmann2, 7, Markus Weiler1, 7, Peer Wulff1, Sebastian Jessberger1, Uwe Konietzko3, Joey Scafidi4, Ursula Staubli4, Jürgen Bereiter-Hahn5, Klaus Strebhardt6 and Dietmar Kuhl1 |
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1 Zentrum für Molekulare Neurobiologie (ZMNH), University of Hamburg, Martinistra e 52, D-20246 Hamburg, Germany2 Present address: Artemis Pharmaceuticals GmbH, Neurather Ring 1, D-51063 Cologne, Germany 3 Present address: The Salk Institute for Biological Studies, Laboratory of Genetics, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA 4 Center for Neural Science, New York University, New York, NY 10003, USA 5 Department of Biology, J.W.Goethe-Universität, Marie-Curie-Stra e 9, D-60439 Frankfurt, Germany6 Department of Obstetrics and Gynecology, J.W.Goethe-Universität, Theodor-Stern-Kai 7, D-60590 Frankfurt, Germany 7 G.Kauselmann and M.Weiler contributed equally to this work To whom correspondence should be addressed Dietmar Kuhl, kuhl@plexus.uke.uni-hamburg.de Received 9 June 1999; Revised 27 August 1999; Accepted 27 August 1999. |
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| Abstract |
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| 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 Ca2+- and integrin-binding protein. Together, these studies suggest a novel signal transduction mechanism in the stabilization of long-term synaptic plasticity. |
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| Keywords: gene induction, hippocampus, integrin, LTP, seizure |
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