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Postsynaptic Y654 dephosphorylation of β‐catenin modulates presynaptic vesicle turnover through increased n‐cadherin‐mediated transsynaptic signaling
Author(s) -
Chen ChinYi,
Chen YiTing,
Wang JenYeu,
Huang YiShuian,
Tai ChinYin
Publication year - 2017
Publication title -
developmental neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.716
H-Index - 129
eISSN - 1932-846X
pISSN - 1932-8451
DOI - 10.1002/dneu.22411
Subject(s) - postsynaptic potential , biology , dephosphorylation , microbiology and biotechnology , neuroscience , synaptic vesicle , phosphorylation , vesicle , biochemistry , phosphatase , receptor , membrane
ABSTRACT Synaptic adhesion molecules, which coordinately control structural and functional changes at both sides of synapses, are important for synaptogenesis and synaptic plasticity. Because they physically form homophilic or heterophilic adhesions across synaptic junctions, these molecules can initiate transsynaptic communication in both anterograde and retrograde directions. Using optical imaging approaches, we investigated whether an increase in postsynaptic N‐cadherin could correspondingly alter the function of connected presynaptic terminals. Postsynaptic expression of β‐catenin Y654F, a phosphorylation‐defective form with enhanced binding to N‐cadherin, is sufficient to increase postsynaptic surface levels of N‐cadherin and consequently promote presynaptic reorganizations. Such reorganizations include increases in the densities of the synaptic vesicle protein, Synaptotagmin 1 and the active zone scaffold protein, Bassoon, the number of active boutons and the size of the total recycling vesicle pool. In contrast, synaptic vesicle turnover is significantly impaired, preventing the exchange of synaptic vesicles with adjacent boutons. Together, N‐cadherin‐mediated retrograde signaling, governed by phosphoregulation of postsynaptic β‐catenin Y654, coordinately modulates presynaptic vesicle dynamics to enhance synaptic communication in mature neurons. © 2016 Wiley Periodicals, Inc. Develop Neurobiol 77: 61–74, 2017