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The Journal of Neuroscience, April 29, 2009, 29(17):5435-5442; doi:10.1523/JNEUROSCI.0835-09.2009

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Cellular/Molecular
{delta}-Catenin Regulates Spine and Synapse Morphogenesis and Function in Hippocampal Neurons during Development

Jyothi Arikkath,1 I-Feng Peng,2 Yu Gie Ng,1 Inbal Israely,3 Xin Liu,3,4,5 Erik M. Ullian,2 and Louis F. Reichardt1

Departments of 1Physiology and 2Ophthalmology, Beckman Vision Center, University of California, San Francisco, San Francisco, California 94143, and Departments of 3Molecular and Medical Pharmacology and 4Pathology and Laboratory Medicine and 5Brain Research Institute, University of California, Los Angeles, Los Angeles, California 90095

Correspondence should be addressed to either Jyothi Arikkath or Louis F. Reichardt, Department of Physiology, University of California, San Francisco, 1550 Fourth Street, San Francisco, CA 94143. Email: Jyothi.arikkath{at}ucsf.edu or Email: louis.reichardt{at}ucsf.edu

The maintenance of spine and synapse number during development is critical for neuronal circuit formation and function. Here we show that {delta}-catenin, a component of the cadherin-catenin cell adhesion complex, regulates spine and synapse morphogenesis during development. Genetic ablation or acute knockdown of {delta}-catenin leads to increases in spine and synapse density, accompanied by a decrease in tetrodotoxin induced spine plasticity. Our results indicate that {delta}-catenin may mediate conversion of activity-dependent signals to morphological spine plasticity. The functional role of {delta}-catenin in regulating spine density does not require binding to cadherins, but does require interactions with PDZ domain-containing proteins. We propose that the perturbations in spine and synaptic structure and function observed after depletion of {delta}-catenin during development may contribute to functional alterations in neural circuitry, the cognitive deficits observed in mutant mice, and the mental retardation pathology of Cri-du-chat syndrome.

Received Feb. 18, 2009; revised March 11, 2009; accepted March 23, 2009.

Correspondence should be addressed to either Jyothi Arikkath or Louis F. Reichardt, Department of Physiology, University of California, San Francisco, 1550 Fourth Street, San Francisco, CA 94143. Email: Jyothi.arikkath{at}ucsf.edu or Email: louis.reichardt{at}ucsf.edu






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