Erbin controls dendritic morphogenesis by regulating localization of δ-catenin

Jyothi Arikkath, Inbal Israely, Yanmei Tao, Lin Mei, Xin Liu, Louis F. Reichardt

Research output: Contribution to journalArticlepeer-review

37 Scopus citations


The LAP [leucine-rich and postsynaptic density-95/Discs large/zona occludens-1 (PDZ)] protein erbin and δ-catenin, a component of the cadherin- catenin cell adhesion complex, are highly expressed in neurons and associate through PDZ-mediated interaction, but have incompletely characterized neuronal functions. We show that short hairpin RNA-mediated knockdown of erbin and knockdown or genetic ablation of δ-catenin severely impaired dendritic morphogenesis in hippocampal neurons. Simultaneous loss of erbin and δ-catenin does not enhance severity of this phenotype. The dendritic phenotype observed after erbin depletion is rescued by overexpression of δ-catenin and requires a domain in δ-catenin that has been shown to regulate dendritic branching. Knockdown of δ-catenin cannot be rescued by overexpression of erbin, indicating that erbin is upstream of δ-catenin. δ-Catenin-null neurons have no alterations in global levels of active Rac1/RhoA. Knockdown of erbin results in alterations in localization of δ-catenin. These results suggest a critical role for erbin in regulating dendritic morphogenesis by maintaining appropriate localization of δ-catenin.

Original languageEnglish (US)
Pages (from-to)7047-7056
Number of pages10
JournalJournal of Neuroscience
Issue number28
StatePublished - Jul 9 2008
Externally publishedYes


  • Dendrite
  • Erbin
  • LAP proteins
  • Localization
  • PDZ
  • δ-catenin

ASJC Scopus subject areas

  • Neuroscience(all)


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