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Ectodomain shedding of nectin‐1 regulates the maintenance of dendritic spine density
Author(s) -
Lim Seung T.,
Chang Allison,
Giuliano Rita E.,
Federoff Howard J.
Publication year - 2012
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2011.07592.x
Subject(s) - ectodomain , nectin , microbiology and biotechnology , biology , dendritic spine , dendritic filopodia , cell adhesion molecule , adherens junction , cadherin , cell adhesion , hippocampal formation , cell , neuroscience , biochemistry , receptor
J. Neurochem. (2012) 120 , 741–751. Abstract Synaptic remodeling has been postulated as a mechanism underlying synaptic plasticity and cell adhesion molecules are thought to contribute to this process. We examined the role of nectin‐1 ectodomain shedding on synaptogenesis in cultured rat hippocampal neurons. Nectins are Ca 2+ ‐independent immunoglobulin‐like adhesion molecules, involved in cell‐cell adherens junctions. Herein, we show that the processing of nectin‐1 occurs by multiple endoproteolytic steps both in vivo and in vitro . We identified regions containing two distinct cleavage sites within the ectodomain of nectin‐1. By alanine scanning mutagenesis, two point mutations that disrupt nectin‐1 ectodomain cleavage events were identified. Expression of these mutants significantly alters the density of dendritic spines. These findings suggest that ectodomain shedding of nectin‐1 regulates dendritic spine density and related synaptic functions.