EphB/syndecan-2 signaling in dendritic spine morphogenesis.

Research output: Contribution to journalJournal articleResearchpeer-review

I M Ethell, F Irie, M S Kalo, J R Couchman, E B Pasquale, Y Yamaguchi

We previously reported that the cell surface proteoglycan syndecan-2 can induce dendritic spine formation in hippocampal neurons. We demonstrate here that the EphB2 receptor tyrosine kinase phosphorylates syndecan-2 and that this phosphorylation event is crucial for syndecan-2 clustering and spine formation. Syndecan-2 is tyrosine phosphorylated and forms a complex with EphB2 in mouse brain. Dominant-negative inhibition of endogenous EphB receptor activities blocks clustering of endogenous syndecan-2 and normal spine formation in cultured hippocampal neurons. This is the first evidence that Eph receptors play a physiological role in dendritic spine morphogenesis. Our observations suggest that spine morphogenesis is triggered by the activation of Eph receptors, which causes tyrosine phosphorylation of target molecules, such as syndecan-2, in presumptive spines.
Original languageEnglish
JournalNeuron
Volume31
Issue number6
Pages (from-to)1001-13
Number of pages12
ISSN0896-6273
Publication statusPublished - 2001

Bibliographical note

Keywords: Animals; Cells, Cultured; Dendrites; Excitatory Postsynaptic Potentials; Hippocampus; Membrane Glycoproteins; Mice; Morphogenesis; Mutagenesis, Site-Directed; Nerve Tissue Proteins; Neuronal Plasticity; Phosphorylation; Phosphotyrosine; Protein Processing, Post-Translational; Proteoglycans; Rats; Receptor Protein-Tyrosine Kinases; Receptor, EphB2; Signal Transduction; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization; Syndecan-2; Transfection

ID: 5162904