Abstract
δ-Catenin is a component of the cadherin-catenin cell adhesion complex and its loss has been implicated in the mental retardation associated with the Cri du chat syndrome. We have previously demonstrated that loss of δ-catenin in a murine model during development results in excessive spine and synaptic density and function. In order to examine the role of potential molecules that might cooperate with δ-catenin to regulate spine density, we focused on Mef2. Our data demonstrate that while loss of δ-catenin does not alter the expression levels of endogenous Mef2, expression of Mef2 in neurons that are knocked down for δ-catenin promotes spine elimination. These results establish a molecular mechanism by which excessive spines in the absence of δ-catenin may be eliminated and may point toward pharmacological therapy for the Cri du chat syndrome.
Original language | English (US) |
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Pages (from-to) | 10-13 |
Number of pages | 4 |
Journal | Neuroscience Letters |
Volume | 536 |
Issue number | 1 |
DOIs | |
State | Published - Mar 1 2013 |
Keywords
- Mef2
- Spine
- Spine elimination
- δ-Catenin
ASJC Scopus subject areas
- Neuroscience(all)