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First published online 1 March 2005
doi: 10.1242/jcs.01711

Journal of Cell Science 118, 1279-1290 (2005)
Published by The Company of Biologists 2005
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Research Article

A dynamin-3 spliced variant modulates the actin/cortactin-dependent morphogenesis of dendritic spines

Noah W. Gray1,*, Anne E. Kruchten2, Jing Chen2 and Mark A. McNiven1,2,{ddagger}

1 Molecular Neuroscience Program and Graduate School, Mayo Clinic, Rochester, MN 55905, USA
2 Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN 55905, USA

{ddagger} Author for correspondence (e-mail: mmcniven{at}mayo.edu)

Accepted 7 January 2005

Immature dendrites extend many actin-rich filopodial structures that can be replaced by synapse-containing dendritic spines as the neuron matures. The large GTPase dynamin-3 (Dyn3) is a component of the postsynapse in hippocampal neurons but its function is undefined. Here, we demonstrate that a specific Dyn3 variant (Dyn3baa) promotes the formation of immature dendritic filopodia in cultured neurons. This effect is dependent upon Dyn3 GTPase activity and a direct interaction with the F-actin-binding protein cortactin. Consistent with these findings, Dyn3baa binds to cortactin with a 200% higher affinity than Dyn3aaa, a near identical isoform that does not induce dendritic filopodia when expressed in cultured neurons. Finally, levels of Dyn3baa-encoding mRNA are tightly regulated during neuronal maturation and are markedly upregulated during synaptogenesis. Together, these findings provide the first evidence that an enhanced interaction between a specific Dyn3 splice variant and cortactin modulate actin-membrane dynamics in developing neurons to regulate the morphogenesis of dendritic spines.

Key words: Dynamin, Cortactin, Filopodia, Actin, Neuron




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