scholarly journals The Planar Cell Polarity Transmembrane Protein Vangl2 Promotes Dendrite, Spine and Glutamatergic Synapse Formation in the Mammalian Forebrain

2016 ◽  
Vol 2 (2) ◽  
pp. 107-114 ◽  
Author(s):  
Nathan D. Okerlund ◽  
Robert E. Stanley ◽  
Benjamin N.R. Cheyette
Keyword(s):  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Synapse Formation ◽  
Transmembrane Protein ◽  
Glutamatergic Synapse ◽  
Dendrite Spine

scholarly journals Apical restriction of the planar cell polarity component VANGL in pancreatic ducts is required to maintain epithelial integrity

2019 ◽  
Author(s):  
Lydie Flasse ◽  
Siham Yennek ◽  
Cédric Cortijo ◽  
Irene Seijo Barandiaran ◽  
Marine R-C Kraus ◽  
...  
Keyword(s):  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Transmembrane Protein ◽  
Pancreatic Ducts ◽  
Apical Surface ◽  
Epithelial Integrity ◽  
Ductal Cells ◽  
And Function ◽  
Rock Activity

ABSTRACTCell polarity is essential for the architecture and function of numerous epithelial tissues. Here we show how planar cell polarity (PCP), so far studied principally in flat epithelia, is deployed during the morphogenesis of a tubular organ. Using the mammalian pancreas as a model, we report that components of the core PCP pathway such as the transmembrane protein Van Gogh-like (VANGL), are progressively apically-restricted. VANGL expression becomes asymmetrically localized at the apical surface of ductal cells, revealing a planar polarization of the pancreatic duct. We further show that restricting VANGL to these discrete sites of expression is crucial for epithelial integrity. Expansion of expression on basolateral membranes of the progenitors leads to their death and extrusion from the epithelium, as previously observed for perturbations of apico-basal polarity. Using organoids and in vivo analyses, we show that cell elimination is induced by a decrease of Rock activity via Dishevelled.

scholarly journals Protecting synapses from amyloid β-associated degeneration by manipulations of Wnt/planar cell polarity signaling

2020 ◽  
Author(s):  
Bo Feng ◽  
Andiara E. Freitas ◽  
Runyi Tian ◽  
Yeo Rang Lee ◽  
Akumbir S. Grewal ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Planar Cell Polarity ◽  
Synapse Formation ◽  
Amyloid Β ◽  
Glutamatergic Synapse ◽  
Aβ Oligomers ◽  
Synapse Loss ◽  
Synapse Maintenance ◽  
Pcp Signaling

ABSTRACTSynapse loss is an early event in Alzheimer’s disease and is thought to be associated with amyloid pathology and caused by Amyloid β (Aβ) oligomers. Whether and how Aβ oligomers directly target signaling pathways for glutamatergic synapse maintenance is unknown. Glutamatergic synapse development is controlled by the opposing functions of Celsr3 and Vangl2, core components of the Wnt/planar cell polarity (PCP) signaling pathway, functioning directly in the synapses. Celsr3 promotes synapse formation, whereas Vangl2 inhibits synapse formation. Here we show that oligomeric Aβ binds to Celsr3 and assists Vangl2 in disassembling synapses by disrupting the intercellular Celsr3/Frizzled3-Celsr3 complex, essential for PCP signaling. Together with Vangl2, a Wnt receptor, Ryk, is also required for Aβ oligomer-induced synapse loss in a mouse model of Alzheimer’s disease, 5XFAD, where conditional Ryk knockout protected synapses and preserved cognitive function. Our study reveals a fine balance of Wnt/PCP signaling components in glutamatergic synapse maintenance and suggests that overproduced Aβ oligomers may lead to excessive synapse loss by tipping this balance. Together with previous reports that an inhibitor of Wnt/Ryk signaling, WIF1, is found reduced in Alzheimer’s disease patients, our results suggest that the imbalance of PCP signaling in these patients may contribute to synapse loss in Alzheimer’s disease and manipulating Wnt/PCP signaling may preserve synapses and cognitive function.

scholarly journals Planar Cell Polarity: The Frizzled Homophobic Signal

2019 ◽  
Author(s):  
José-Eduardo Gomes
Keyword(s):  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Spatial Information ◽  
Transmembrane Protein ◽  
Adjacent Cell ◽  
Signaling Mechanism ◽  
Insect Wing ◽  
Crucial Feature ◽  
Pcp Signaling ◽  
Core Genes

The cell’s capacity to integrate and respond to spatial information is a crucial feature of morphogenesis and development. The Planar Cell Polarity (PCP) pathway is a signaling mechanism, widely conserved across metazoans, providing spatial orientation along the plane of an epithelium in morphogenic processes ranging from insect wing patterning to mammalian cochleae. Although the core genes involved in the PCP pathway have been molecularly identified in the 1990s, the PCP signaling mechanism remains controversial. In this article I discuss the main players and previous models of PCP signaling reported in the literature, and propose a new model. According to it PCP is established through an homophobic signal by transmembrane protein Frizzled (Fz): 1) a Fz signal in one cell repeals Fz itself in the adjacent cell, thereby generating symmetry breaking; 2) the instructive PCP signal is conveyed through Fz interaction with atypical cadherin Flamingo (Fmi). More broadly, homophobic signaling may represent a novel mechanism for cell-cell signaling of spatial information through modulation of cell adhesion rather than canonical ligand-receptor binding.

scholarly journals The Wnt/Planar Cell Polarity Pathway Component Vangl2 Induces Synapse Formation through Direct Control of N-Cadherin

Cell Reports ◽  
2014 ◽  
Vol 6 (5) ◽  
pp. 916-927 ◽  
Author(s):  
Tadahiro Nagaoka ◽  
Riuko Ohashi ◽  
Ayumu Inutsuka ◽  
Seiko Sakai ◽  
Nobuyoshi Fujisawa ◽  
...  
Keyword(s):  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Synapse Formation ◽  
Direct Control ◽  
Planar Cell Polarity Pathway
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