Ringmaster Of Craniofacial Development- Neural Crest Cell

10.5580/13d9 ◽  
2011 ◽  
Vol 9 (2) ◽  
2011 ◽  
Vol 357 (1) ◽  
pp. 269-281 ◽  
Author(s):  
Christopher W. Johnson ◽  
Laura Hernandez-Lagunas ◽  
Weiguo Feng ◽  
Vida Senkus Melvin ◽  
Trevor Williams ◽  
...  

2010 ◽  
Vol 344 (1) ◽  
pp. 447
Author(s):  
Christopher W. Johnson ◽  
Weiguo Feng ◽  
Trevor Williams ◽  
Kristin Artinger

genesis ◽  
2015 ◽  
Vol 53 (10) ◽  
pp. 660-667 ◽  
Author(s):  
Eric C. Swindell ◽  
Qiuping Yuan ◽  
Lorena E. Maili ◽  
Bhavna Tandon ◽  
Daniel S. Wagner ◽  
...  

2013 ◽  
Vol 383 (2) ◽  
pp. 186-200 ◽  
Author(s):  
Sophie Wiszniak ◽  
Samuela Kabbara ◽  
Rachael Lumb ◽  
Michaela Scherer ◽  
Genevieve Secker ◽  
...  

Development ◽  
2001 ◽  
Vol 128 (8) ◽  
pp. 1253-1264 ◽  
Author(s):  
V. Brault ◽  
R. Moore ◽  
S. Kutsch ◽  
M. Ishibashi ◽  
D.H. Rowitch ◽  
...  

('bgr;)-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of (β)-catenin during brain morphogenesis, by specifically inactivating the (β)-catenin gene in the region of Wnt1 expression. To achieve this, mice with a conditional ('floxed') allele of (β)-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of Wnt1 regulatory sequences. (β)-catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional Wnt1 knockout (Wnt1(−)(/)(−)), suggesting that Wnt1 acts through (β)-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack Wnt1, indicates a role for (β)-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (β)-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of (β)-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of (β)-catenin in morphogenetic processes during brain and craniofacial development.


2020 ◽  
Vol 11 ◽  
Author(s):  
Elizabeth N. Schock ◽  
Carole LaBonne

Sox transcription factors play many diverse roles during development, including regulating stem cell states, directing differentiation, and influencing the local chromatin landscape. Of the twenty vertebrate Sox factors, several play critical roles in the development the neural crest, a key vertebrate innovation, and the subsequent formation of neural crest-derived structures, including the craniofacial complex. Herein, we review the specific roles for individual Sox factors during neural crest cell formation and discuss how some factors may have been essential for the evolution of the neural crest. Additionally, we describe how Sox factors direct neural crest cell differentiation into diverse lineages such as melanocytes, glia, and cartilage and detail their involvement in the development of specific craniofacial structures. Finally, we highlight several SOXopathies associated with craniofacial phenotypes.


2012 ◽  
Vol 363 (1) ◽  
pp. 332
Author(s):  
Christopher W. Johnson ◽  
Laura Hernandez-Lagunas ◽  
Weiguo Feng ◽  
Vida Senkus Melvin ◽  
Trevor Williams ◽  
...  

2009 ◽  
Vol 333 (1) ◽  
pp. 161-172 ◽  
Author(s):  
Eugenia C. Olesnicky Killian ◽  
Denise A. Birkholz ◽  
Kristin Bruk Artinger

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