Neural crest-derived mesenchymal cells require Wnt signaling for their development and drive invagination of the telencephalic midline.

Embryonic neural crest cells contribute to the development of the craniofacial mesenchyme, forebrain meninges and perivascular cells. In this study, we investigated the function of ß-catenin signaling in neural crest cells abutting the dorsal forebrain during development. In the absence of ß-catenin...

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Main Authors: Youngshik Choe, Konstantinos S Zarbalis, Samuel J Pleasure
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3916303?pdf=render
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spelling doaj-48bc6cfd3fc44be8af73c77a76df753b2020-11-25T01:46:28ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0192e8602510.1371/journal.pone.0086025Neural crest-derived mesenchymal cells require Wnt signaling for their development and drive invagination of the telencephalic midline.Youngshik ChoeKonstantinos S ZarbalisSamuel J PleasureEmbryonic neural crest cells contribute to the development of the craniofacial mesenchyme, forebrain meninges and perivascular cells. In this study, we investigated the function of ß-catenin signaling in neural crest cells abutting the dorsal forebrain during development. In the absence of ß-catenin signaling, neural crest cells failed to expand in the interhemispheric region and produced ectopic smooth muscle cells instead of generating dermal and calvarial mesenchyme. In contrast, constitutive expression of stabilized ß-catenin in neural crest cells increased the number of mesenchymal lineage precursors suggesting that ß-catenin signaling is necessary for the expansion of neural crest-derived mesenchymal cells. Interestingly, the loss of neural crest-derived mesenchymal stem cells (MSCs) leads to failure of telencephalic midline invagination and causes ventricular system defects. This study shows that ß-catenin signaling is required for the switch of neural crest cells to MSCs and mediates the expansion of MSCs to drive the formation of mesenchymal structures of the head. Furthermore, loss of these structures causes striking defects in forebrain morphogenesis.http://europepmc.org/articles/PMC3916303?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Youngshik Choe
Konstantinos S Zarbalis
Samuel J Pleasure
spellingShingle Youngshik Choe
Konstantinos S Zarbalis
Samuel J Pleasure
Neural crest-derived mesenchymal cells require Wnt signaling for their development and drive invagination of the telencephalic midline.
PLoS ONE
author_facet Youngshik Choe
Konstantinos S Zarbalis
Samuel J Pleasure
author_sort Youngshik Choe
title Neural crest-derived mesenchymal cells require Wnt signaling for their development and drive invagination of the telencephalic midline.
title_short Neural crest-derived mesenchymal cells require Wnt signaling for their development and drive invagination of the telencephalic midline.
title_full Neural crest-derived mesenchymal cells require Wnt signaling for their development and drive invagination of the telencephalic midline.
title_fullStr Neural crest-derived mesenchymal cells require Wnt signaling for their development and drive invagination of the telencephalic midline.
title_full_unstemmed Neural crest-derived mesenchymal cells require Wnt signaling for their development and drive invagination of the telencephalic midline.
title_sort neural crest-derived mesenchymal cells require wnt signaling for their development and drive invagination of the telencephalic midline.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2014-01-01
description Embryonic neural crest cells contribute to the development of the craniofacial mesenchyme, forebrain meninges and perivascular cells. In this study, we investigated the function of ß-catenin signaling in neural crest cells abutting the dorsal forebrain during development. In the absence of ß-catenin signaling, neural crest cells failed to expand in the interhemispheric region and produced ectopic smooth muscle cells instead of generating dermal and calvarial mesenchyme. In contrast, constitutive expression of stabilized ß-catenin in neural crest cells increased the number of mesenchymal lineage precursors suggesting that ß-catenin signaling is necessary for the expansion of neural crest-derived mesenchymal cells. Interestingly, the loss of neural crest-derived mesenchymal stem cells (MSCs) leads to failure of telencephalic midline invagination and causes ventricular system defects. This study shows that ß-catenin signaling is required for the switch of neural crest cells to MSCs and mediates the expansion of MSCs to drive the formation of mesenchymal structures of the head. Furthermore, loss of these structures causes striking defects in forebrain morphogenesis.
url http://europepmc.org/articles/PMC3916303?pdf=render
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AT konstantinosszarbalis neuralcrestderivedmesenchymalcellsrequirewntsignalingfortheirdevelopmentanddriveinvaginationofthetelencephalicmidline
AT samueljpleasure neuralcrestderivedmesenchymalcellsrequirewntsignalingfortheirdevelopmentanddriveinvaginationofthetelencephalicmidline
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