scholarly journals Face off against ROS: Tcof1 /Treacle safeguards neuroepithelial cells and progenitor neural crest cells from oxidative stress during craniofacial development

2016 ◽  
Vol 58 (7) ◽  
pp. 577-585 ◽  
Author(s):  
Daisuke Sakai ◽  
Paul A. Trainor
Keyword(s):  
Oxidative Stress ◽  
Neural Crest ◽  
Neural Crest Cells ◽  
Craniofacial Development ◽  
Neuroepithelial Cells

scholarly journals Wolf-Hirschhorn Syndrome-Associated Genes Are Enriched in Motile Neural Crest Cells and Affect Craniofacial Development in Xenopus laevis

2019 ◽  
Vol 10 ◽  
Author(s):  
Alexandra Mills ◽  
Elizabeth Bearce ◽  
Rachael Cella ◽  
Seung Woo Kim ◽  
Megan Selig ◽  
...  
Keyword(s):  
Xenopus Laevis ◽  
Neural Crest ◽  
Neural Crest Cells ◽  
Craniofacial Development

scholarly journals Cis‐ control of Six1 expression in neural crest cells during craniofacial development

2019 ◽  
Vol 248 (12) ◽  
pp. 1264-1272 ◽  
Author(s):  
Zhaoming Wu ◽  
Yanxia Rao ◽  
Sushan Zhang ◽  
Eun‐Jung Kim ◽  
Shinya Oki ◽  
...  
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Craniofacial Development

scholarly journals Cranial neural crest cells on the move: Their roles in craniofacial development

2010 ◽  
Vol 155 (2) ◽  
pp. 270-279 ◽  
Author(s):  
Dwight R. Cordero ◽  
Samantha Brugmann ◽  
Yvonne Chu ◽  
Ruchi Bajpai ◽  
Maryam Jame ◽  
...  
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Craniofacial Development ◽  
Cranial Neural Crest ◽  
Cranial Neural Crest Cells

Specification and Patterning of Neural Crest Cells During Craniofacial Development

2005 ◽  
Vol 66 (4) ◽  
pp. 266-280 ◽  
Author(s):  
Paul A. Trainor
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Craniofacial Development

Neural crest emigration from the neural tube depends on regulated cadherin expression

Development ◽  
1998 ◽  
Vol 125 (15) ◽  
pp. 2963-2971 ◽  
Author(s):  
S. Nakagawa ◽  
M. Takeichi
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Critical Role ◽  
Neural Crest Cells ◽  
Migration Pattern ◽  
Dominant Negative ◽  
Expression Vectors ◽  
Neural Tubes ◽  
Neuroepithelial Cells

During the emergence of neural crest cells from the neural tube, the expression of cadherins dynamically changes. In the chicken embryo, the early neural tube expresses two cadherins, N-cadherin and cadherin-6B (cad6B), in the dorsal-most region where neural crest cells are generated. The expression of these two cadherins is, however, downregulated in the neural crest cells migrating from the neural tube; they instead begin expressing cadherin-7 (cad7). As an attempt to investigate the role of these changes in cadherin expression, we overexpressed various cadherin constructs, including N-cadherin, cad7, and a dominant negative N-cadherin (cN390), in neural crest-generating cells. This was achieved by injecting adenoviral expression vectors encoding these molecules into the lumen of the closing neural tube of chicken embryos at stage 14. In neural tubes injected with the viruses, efficient infection was observed at the neural crest-forming area, resulting in the ectopic cadherin expression also in migrating neural crest cells. Notably, the distribution of neural crest cells with the ectopic cadherins changed depending on which constructs were expressed. Many crest cells failed to escape from the neural tube when N-cadherin or cad7 was overexpressed. Moreover, none of the cells with these ectopic cadherins migrated along the dorsolateral (melanocyte) pathway. When these samples were stained for Mitf, an early melanocyte marker, positive cells were found accumulated within the neural tube, suggesting that the failure of their migration was not due to differentiation defects. In contrast to these phenomena, cells expressing non-functional cadherins exhibited a normal migration pattern. Thus, the overexpression of a neuroepithelial cadherin (N-cadherin) and a crest cadherin (cad7) resulted in the same blocking effect on neural crest segregation from neuroepithelial cells, especially for melanocyte precursors. These findings suggest that the regulation of cadherin expression or its activity at the neural crest-forming area plays a critical role in neural crest emigration from the neural tube.

scholarly journals mTOR acts as a pivotal signaling hub for neural crest cells during craniofacial development

PLoS Genetics ◽  
2018 ◽  
Vol 14 (7) ◽  
pp. e1007491 ◽  
Author(s):  
Xuguang Nie ◽  
Jinxuan Zheng ◽  
Christopher L. Ricupero ◽  
Ling He ◽  
Kai Jiao ◽  
...  
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Craniofacial Development

Prenatal Craniofacial Development: New Insights On Normal and Abnormal Mechanisms

1995 ◽  
Vol 6 (1) ◽  
pp. 25-79 ◽  
Author(s):  
M.C. Johnston ◽  
P.T. Bronsky
Keyword(s):  
Retinoic Acid ◽  
Animal Models ◽  
Neural Crest ◽  
Regulatory Gene ◽  
Neural Crest Cells ◽  
Craniofacial Development ◽  
Neural Plate ◽  
Treacher Collins Syndrome ◽  
Abnormal Development ◽  
Dentofacial Deformities

Technical advances are radically altering our concepts of normal prenatal craniofacial development. These include concepts of germ layer formation, the establishment of the initial head plan in the neural plate, and the manner in which head segmentation is controlled by regulatory (homeobox) gene activity in neuromeres and their derived neural crest cells. There is also a much better appreciation of ways in which new cell associations are established. For example, the associations are achieved by neural crest cells primarily through cell migration and subsequent cell interactions that regulate induction, growth, programmed cell death, etc. These interactions are mediated primarily by two groups of regulatory molecules: "growth factors" ( e.g., FGF and TGFa) and the so-called steroid/thyroid/retinoic acid superfamily. Considerable advances have been made with respect to our understanding of the mechanisms involved in primary and secondary palate formation, such as growth, morphogenetic movements, and the fusion/merging phenomenon. Much progress has been made on the mechanisms involved in the final differentiation of skeletal tissues. Molecular genetics and animal models for human malformations are providing many insights into abnormal development. A mouse model for the fetal alcohol syndrome (FAS), a mild form of holoprosencephaly, demonstrates a mid-line anterior neural plate deficiency which leads to olfactory placodes being positioned too close to the mid-line, and other secondary changes. Work on animal models for the retinoic acid syndrome (RAS) shows that there is major involvement of neural crest cells. There is also major crest cell involvement in similar syndromes, apparently including hemifacial microsomia. Later administration of retinoic acid prematurely and excessively kills ganglionic placodal cells and leads to a malformation complex virtually identical to the Treacher Collins syndrome. Most clefts of the lip and/or palate appear to have a multifactorial etiology. Genetic variations in TGFas, RARas, NADH dehydrogenase, an enzyme involved in oxidative metabolism, and cytochrome P-450, a detoxifying enzyme, have been implicated as contributing genetic factors. Cigarette smoking, with the attendant hypoxia, is a probable contributing environmental factor. It seems likely that few clefts involve single major genes. In most cases, the pathogenesis appears to involve inadequate contact and/or fusion of the facial prominences or palatal shelves. Specific mutations in genes for different FGF receptor molecules have been identified for achondroplasia and Crouzon's syndrome, and in a regulatory gene (Msx2) for one type of craniosynostosis. Poorly co-ordinated control of form and size of structures, or groups of structures (e.g., teeth and jaws), by regulatory genes should do much to explain the very frequent "mismatches" found in malocclusions and other dentofacial "deformities". Future directions for research, including possibilities for prevention, are discussed.

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