A dual shaping mechanism for postsynaptic ephrin-B3 as a receptor that sculpts dendrites and synapses

Nan Jie Xu, Suya Sun, Jay R. Gibson, Mark Henkemeyer

Research output: Contribution to journalArticle

48 Citations (Scopus)

Abstract

As the neural network becomes wired, postsynaptic signaling molecules are thought to control the growth of dendrites and synapses. However, how these molecules are coordinated to sculpt postsynaptic structures is less well understood. We find that ephrin-B3, a transmembrane ligand for Eph receptors, functions postsynaptically as a receptor to transduce reverse signals into developing dendrites of mouse hippocampal neurons. Both tyrosine phosphorylationg - dependent GRB4 SH2/SH3 adaptor-mediated signals and PSD-95g - discs largeg - zona occludens-1 (PDZ) domaing - dependent signals are required for inhibition of dendrite branching, whereas only PDZ interactions are necessary for spine formation and excitatory synaptic function. PICK1 and syntenin, two PDZ domain proteins, participate with ephrin-B3 in these postsynaptic activities. PICK1 has a specific role in spine and synapse formation, and syntenin promotes both dendrite pruning and synapse formation to build postsynaptic structures that are essential for neural circuits. The study thus dissects ephrin-B reverse signaling into three distinct intracellular pathways and proteing - protein interactions that mediate the maturation of postsynaptic neurons.

Original languageEnglish (US)
Pages (from-to)1421-1429
Number of pages9
JournalNature Neuroscience
Volume14
Issue number11
DOIs
StatePublished - Nov 2011

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Ephrin-B3
Syntenins
Dendrites
Ephrins
Synapses
Spine
PDZ Domains
Neurons
Neuronal Plasticity
Herpes Zoster
Tyrosine
Proteins
Growth

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

A dual shaping mechanism for postsynaptic ephrin-B3 as a receptor that sculpts dendrites and synapses. / Xu, Nan Jie; Sun, Suya; Gibson, Jay R.; Henkemeyer, Mark.

In: Nature Neuroscience, Vol. 14, No. 11, 11.2011, p. 1421-1429.

Research output: Contribution to journalArticle

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