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.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Yuan Y,Singh D,Arikkath Jdoi
10.1016/j.neulet.2013.01.002subject
Has Abstractpub_date
2013-03-01 00:00:00pages
10-3eissn
0304-3940issn
1872-7972pii
S0304-3940(13)00016-5journal_volume
536pub_type
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