Ringmaster Of Craniofacial Development- Neural Crest Cell

10.5580/13d9 ◽  
2011 ◽  
Vol 9 (2) ◽  
Keyword(s):  
Neural Crest ◽  
Neural Crest Cell ◽  
Craniofacial Development ◽  
Crest Cell

scholarly journals Vgll2a is required for neural crest cell survival during zebrafish craniofacial development

2011 ◽  
Vol 357 (1) ◽  
pp. 269-281 ◽  
Author(s):  
Christopher W. Johnson ◽  
Laura Hernandez-Lagunas ◽  
Weiguo Feng ◽  
Vida Senkus Melvin ◽  
Trevor Williams ◽  
...  
Keyword(s):  
Neural Crest ◽  
Cell Survival ◽  
Neural Crest Cell ◽  
Craniofacial Development ◽  
Crest Cell

scholarly journals Vgl-2a is Required for Neural Crest Cell Survival During Zebrafish Craniofacial Development

2010 ◽  
Vol 344 (1) ◽  
pp. 447
Author(s):  
Christopher W. Johnson ◽  
Weiguo Feng ◽  
Trevor Williams ◽  
Kristin Artinger
Keyword(s):  
Neural Crest ◽  
Cell Survival ◽  
Neural Crest Cell ◽  
Craniofacial Development ◽  
Crest Cell

scholarly journals Crispld2 is required for neural crest cell migration and cell viability during zebrafish craniofacial development

genesis ◽  
2015 ◽  
Vol 53 (10) ◽  
pp. 660-667 ◽  
Author(s):  
Eric C. Swindell ◽  
Qiuping Yuan ◽  
Lorena E. Maili ◽  
Bhavna Tandon ◽  
Daniel S. Wagner ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Viability ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Craniofacial Development ◽  
Neural Crest Cell Migration ◽  
Crest Cell

scholarly journals The ubiquitin ligase Nedd4 regulates craniofacial development by promoting cranial neural crest cell survival and stem-cell like properties

2013 ◽  
Vol 383 (2) ◽  
pp. 186-200 ◽  
Author(s):  
Sophie Wiszniak ◽  
Samuela Kabbara ◽  
Rachael Lumb ◽  
Michaela Scherer ◽  
Genevieve Secker ◽  
...  
Keyword(s):  
Stem Cell ◽  
Neural Crest ◽  
Cell Survival ◽  
Ubiquitin Ligase ◽  
Neural Crest Cell ◽  
Craniofacial Development ◽  
Cranial Neural Crest ◽  
Cranial Neural Crest Cell ◽  
Crest Cell

Inactivation of the (β)-catenin gene by Wnt1-Cre-mediated deletion results in dramatic brain malformation and failure of craniofacial development

Development ◽  
2001 ◽  
Vol 128 (8) ◽  
pp. 1253-1264 ◽  
Author(s):  
V. Brault ◽  
R. Moore ◽  
S. Kutsch ◽  
M. Ishibashi ◽  
D.H. Rowitch ◽  
...  
Keyword(s):  
Neural Crest ◽  
Wnt Signaling Pathway ◽  
Neural Crest Cell ◽  
Craniofacial Development ◽  
Central Component ◽  
Regulatory Sequences ◽  
Brain Malformation ◽  
Cranial Ganglia ◽  
Crest Cell

('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.

scholarly journals Sorting Sox: Diverse Roles for Sox Transcription Factors During Neural Crest and Craniofacial Development

2020 ◽  
Vol 11 ◽  
Author(s):  
Elizabeth N. Schock ◽  
Carole LaBonne
Keyword(s):  
Stem Cell ◽  
Transcription Factors ◽  
Neural Crest ◽  
Cell Formation ◽  
Neural Crest Cell ◽  
Craniofacial Development ◽  
Subsequent Formation ◽  
Crest Cell ◽  
Craniofacial Complex ◽  
And Cartilage

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.

scholarly journals Corrigendum to “Vgll2a is required for neural crest cell survival during zebrafish craniofacial development” [Dev. Biol. 357 (2011) 269–281]

2012 ◽  
Vol 363 (1) ◽  
pp. 332
Author(s):  
Christopher W. Johnson ◽  
Laura Hernandez-Lagunas ◽  
Weiguo Feng ◽  
Vida Senkus Melvin ◽  
Trevor Williams ◽  
...  
Keyword(s):  
Neural Crest ◽  
Cell Survival ◽  
Neural Crest Cell ◽  
Craniofacial Development ◽  
Crest Cell

scholarly journals Wolf-Hirschhorn Syndrome-associated genes are enriched in motile neural crest and affect craniofacial development in Xenopus laevis

2018 ◽  
Author(s):  
Alexandra Mills ◽  
Elizabeth Bearce ◽  
Rachael Cella ◽  
Seung Woo Kim ◽  
Megan Selig ◽  
...  
Keyword(s):  
Cell Migration ◽  
Xenopus Laevis ◽  
Neural Crest ◽  
Developmental Disorder ◽  
Neural Crest Cell ◽  
Craniofacial Development ◽  
Cartilage Formation ◽  
Neural Crest Cell Migration ◽  
Critical Regions ◽  
Crest Cell

Wolf-Hirschhorn Syndrome (WHS) is a human developmental disorder arising from a hemizygous perturbation, typically a microdeletion, on the short arm of chromosome four. In addition to pronounced intellectual disability, seizures, and delayed growth, WHS presents with a characteristic facial dysmorphism and varying prevalence of microcephaly, micrognathia, cartilage malformation in the ear and nose, and facial asymmetries. These affected craniofacial tissues all derive from a shared embryonic precursor, the cranial neural crest, inviting the hypothesis that one or more WHS-affected genes may be critical regulators of neural crest development or migration. To explore this, we characterized expression of multiple genes within or immediately proximal to defined WHS critical regions, across the span of craniofacial development in the vertebrate model system Xenopus laevis. This subset of genes, WHSC1, WHSC2, LETM1, and TACC3, are diverse in their currently-elucidated cellular functions; yet we find that their expression demonstrates shared tissue-specific enrichment within the anterior neural tube, pharyngeal arches, and later craniofacial structures. We examine the ramifications of this by characterizing craniofacial development and neural crest migration following individual gene depletion. We observe that several WHS-associated genes significantly impact facial patterning, cartilage formation, pharyngeal arch migration, and neural crest motility, and can separately contribute to forebrain scaling. Thus, we have determined that numerous genes within and surrounding the defined WHS critical regions potently impact craniofacial patterning, suggesting their role in WHS presentation may stem from essential functions during neural crest-derived tissue formation.Author SummaryWolf-Hirschhorn Syndrome (WHS), a developmental disorder caused by small deletions on chromosome four, manifests with pronounced and characteristic facial malformation. While genetic profiling and case studies provide insights into how broader regions of the genome affect the syndrome’s severity, we lack a key component of understanding its pathology; a basic knowledge of how individual WHS-affected genes function during development. Importantly, many tissues affected by WHS derive from shared embryonic origin, the cranial neural crest. This led us to hypothesize that genes deleted in WHS may hold especially critical roles in this tissue. To this end, we investigated the roles of four WHS-associated genes during neural crest cell migration and facial patterning. We show that during normal development, expression of these genes is enriched in migratory neural crest and craniofacial structures. Subsequently, we examine their functional roles during facial patterning, cartilage formation, and forebrain development, and find that their depletion recapitulates features of WHS craniofacial malformation. Additionally, two of these genes directly affect neural crest cell migration rate. We report that depletion of WHS-associated genes is a potent effector of neural crest-derived tissues, and suggest that this explains why WHS clinical presentation shares so many characteristics with classic neurochristopathies.

scholarly journals A role for chemokine signaling in neural crest cell migration and craniofacial development

2009 ◽  
Vol 333 (1) ◽  
pp. 161-172 ◽  
Author(s):  
Eugenia C. Olesnicky Killian ◽  
Denise A. Birkholz ◽  
Kristin Bruk Artinger
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Craniofacial Development ◽  
Chemokine Signaling ◽  
Neural Crest Cell Migration ◽  
Crest Cell
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