Alk8 is required for neural crest cell formation and development of pharyngeal arch cartilages

2003 ◽  
Vol 228 (4) ◽  
pp. 683-696 ◽  
Author(s):  
T.L. Payne-Ferreira ◽  
P.C. Yelick
Keyword(s):  
Neural Crest ◽  
Cell Formation ◽  
Neural Crest Cell ◽  
Pharyngeal Arch ◽  
Crest Cell

scholarly journals Homocysteine inhibits cardiac neural crest cell formation and morphogenesis in vivo

2003 ◽  
Vol 229 (1) ◽  
pp. 63-73 ◽  
Author(s):  
Brent J. Tierney ◽  
Trang Ho ◽  
Mark V. Reedy ◽  
Philip R. Brauer
Keyword(s):  
Neural Crest ◽  
Cell Formation ◽  
Neural Crest Cell ◽  
Cardiac Neural Crest ◽  
Crest Cell

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 SUMOylation Potentiates ZIC Protein Activity to Influence Murine Neural Crest Cell Specification

2021 ◽  
Vol 22 (19) ◽  
pp. 10437
Author(s):  
Helen M. Bellchambers ◽  
Kristen S. Barratt ◽  
Koula E. M. Diamand ◽  
Ruth M. Arkell
Keyword(s):  
Neural Crest ◽  
Zinc Finger ◽  
Cell Formation ◽  
Neural Crest Cell ◽  
Neural Plate ◽  
Model Organisms ◽  
Protein Activity ◽  
Neural Plate Border ◽  
Canonical Wnt ◽  
Crest Cell

The mechanisms of neural crest cell induction and specification are highly conserved among vertebrate model organisms, but how similar these mechanisms are in mammalian neural crest cell formation remains open to question. The zinc finger of the cerebellum 1 (ZIC1) transcription factor is considered a core component of the vertebrate gene regulatory network that specifies neural crest fate at the neural plate border. In mouse embryos, however, Zic1 mutation does not cause neural crest defects. Instead, we and others have shown that murine Zic2 and Zic5 mutate to give a neural crest phenotype. Here, we extend this knowledge by demonstrating that murine Zic3 is also required for, and co-operates with, Zic2 and Zic5 during mammalian neural crest specification. At the murine neural plate border (a region of high canonical WNT activity) ZIC2, ZIC3, and ZIC5 function as transcription factors to jointly activate the Foxd3 specifier gene. This function is promoted by SUMOylation of the ZIC proteins at a conserved lysine immediately N-terminal of the ZIC zinc finger domain. In contrast, in the lateral regions of the neurectoderm (a region of low canonical WNT activity) basal ZIC proteins act as co-repressors of WNT/TCF-mediated transcription. Our work provides a mechanism by which mammalian neural crest specification is restricted to the neural plate border. Furthermore, given that WNT signaling and SUMOylation are also features of non-mammalian neural crest specification, it suggests that mammalian neural crest induction shares broad conservation, but altered molecular detail, with chicken, zebrafish, and Xenopus neural crest induction.

scholarly journals Tcof1/Treacle is required for neural crest cell formation and proliferation deficiencies that cause craniofacial abnormalities

2006 ◽  
Vol 103 (36) ◽  
pp. 13403-13408 ◽  
Author(s):  
J. Dixon ◽  
N. C. Jones ◽  
L. L. Sandell ◽  
S. M. Jayasinghe ◽  
J. Crane ◽  
...  
Keyword(s):  
Neural Crest ◽  
Cell Formation ◽  
Neural Crest Cell ◽  
Craniofacial Abnormalities ◽  
Crest Cell

scholarly journals Msx1 haploinsufficiency modifies the Pax9-deficient cardiovascular phenotype

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ramada R. Khasawneh ◽  
Ralf Kist ◽  
Rachel Queen ◽  
Rafiqul Hussain ◽  
Jonathan Coxhead ◽  
...  
Keyword(s):  
Neural Crest ◽  
Aortic Arch ◽  
Thyroid Cartilage ◽  
Neural Crest Cell ◽  
Pharyngeal Arch ◽  
Palate Development ◽  
The Third ◽  
Pharyngeal Endoderm ◽  
Cardiovascular Defects ◽  
Crest Cell

Abstract Background Successful embryogenesis relies on the coordinated interaction between genes and tissues. The transcription factors Pax9 and Msx1 genetically interact during mouse craniofacial morphogenesis, and mice deficient for either gene display abnormal tooth and palate development. Pax9 is expressed specifically in the pharyngeal endoderm at mid-embryogenesis, and mice deficient for Pax9 on a C57Bl/6 genetic background also have cardiovascular defects affecting the outflow tract and aortic arch arteries giving double-outlet right ventricle, absent common carotid arteries and interruption of the aortic arch. Results In this study we have investigated both the effect of a different genetic background and Msx1 haploinsufficiency on the presentation of the Pax9-deficient cardiovascular phenotype. Compared to mice on a C57Bl/6 background, congenic CD1-Pax9–/– mice displayed a significantly reduced incidence of outflow tract defects but aortic arch defects were unchanged. Pax9–/– mice with Msx1 haploinsufficiency, however, have a reduced incidence of interrupted aortic arch, but more cases with cervical origins of the right subclavian artery and aortic arch, than seen in Pax9–/– mice. This alteration in arch artery defects was accompanied by a rescue in third pharyngeal arch neural crest cell migration and smooth muscle cell coverage of the third pharyngeal arch arteries. Although this change in phenotype could theoretically be compatible with post-natal survival, using tissue-specific inactivation of Pax9 to maintain correct palate development whilst inducing the cardiovascular defects was unable to prevent postnatal death in the mutant mice. Hyoid bone and thyroid cartilage formation were abnormal in Pax9–/– mice. Conclusions Msx1 haploinsufficiency mitigates the arch artery defects in Pax9–/– mice, potentially by maintaining the survival of the 3rd arch artery through unimpaired migration of neural crest cells to the third pharyngeal arches. With the neural crest cell derived hyoid bone and thyroid cartilage also being defective in Pax9–/– mice, we speculate that the pharyngeal endoderm is a key signalling centre that impacts on neural crest cell behaviour highlighting the ability of cells in different tissues to act synergistically or antagonistically during embryo development.

scholarly journals Dorsalization of the neural tube by the non-neural ectoderm

Development ◽  
1995 ◽  
Vol 121 (7) ◽  
pp. 2099-2106 ◽  
Author(s):  
M.E. Dickinson ◽  
M.A. Selleck ◽  
A.P. McMahon ◽  
M. Bronner-Fraser
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Cell Formation ◽  
Neural Crest Cell ◽  
Neural Tissue ◽  
Cell Types ◽  
Stage 4 ◽  
Slug Expression ◽  
Neural Ectoderm ◽  
Crest Cell

The patterning of cell types along the dorsoventral axis of the spinal cord requires a complex set of inductive signals. While the chordamesoderm is a well-known source of ventralizing signals, relatively little is known about the cues that induce dorsal cell types, including neural crest. Here, we demonstrate that juxtaposition of the non-neural and neural ectoderm is sufficient to induce the expression of dorsal markers, Wnt-1, Wnt-3a and Slug, as well as the formation of neural crest cells. In addition, the competence of neural plate to express Wnt-1 and Wnt-3a appears to be stage dependent, occurring only when neural tissue is taken from stage 8–10 embryos but not from stage 4 embryos, regardless of the age of the non-neural ectoderm. In contrast to the induction of Wnt gene expression, neural crest cell formation and Slug expression can be induced when either stage 4 or stage 8–10 neural plates are placed in contact with the non-neural ectoderm. These data suggest that the non-neural ectoderm provides a signal (or signals) that specifies dorsal cell types within the neural tube, and that the response is dependent on the competence of the neural tissue.

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