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

Noah W. Gray, Anne E. Kruchten, Jing Chen, Mark A. McNiven

Research output: Contribution to journalArticle

45 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1279-1290
Number of pages12
JournalJournal of cell science
Volume118
Issue number6
DOIs
StatePublished - Mar 15 2005

Keywords

  • Actin
  • Cortactin
  • Dynamin
  • Filopodia
  • Neuron

ASJC Scopus subject areas

  • Cell Biology

Fingerprint Dive into the research topics of 'A dynamin-3 spliced variant modulates the actin/cortactin-dependent morphogenesis of dendritic spines'. Together they form a unique fingerprint.

  • Cite this