scholarly journals Making Headway: The Roles of Hox Genes and Neural Crest Cells in Craniofacial Development

2003 ◽  
Vol 3 ◽  
pp. 240-264 ◽  
Author(s):  
Paul A. Trainor
Keyword(s):  
Neural Crest ◽  
Hox Genes ◽  
Neural Crest Cell ◽  
Axial Skeleton ◽  
Craniofacial Development ◽  
Congenital Defects ◽  
Connective Tissues ◽  
Surface Ectoderm ◽  
Head Development ◽  
Tissue Interactions

Craniofacial development is an extraordinarily complex process requiring the orchestrated integration of multiple specialized tissues such as the surface ectoderm, neural crest, mesoderm, and pharyngeal endoderm in order to generate the central and peripheral nervous systems, axial skeleton, musculature, and connective tissues of the head and face. How do the characteristic facial structures develop in the appropriate locations with their correct shapes and sizes, given the widely divergent patterns of cell movements that occur during head development? The patterning information could depend upon localized interactions between the epithelial and mesenchymal tissues or alternatively, the developmental program for the characteristic facial structures could be intrinsic to each individual tissue precursor. Understanding the mechanisms that control vertebrate head development is an important issue since craniofacial anomalies constitute nearly one third of all human congenital defects. This review discusses recent advances in our understanding of neural crest cell patterning and the dynamic nature of the tissue interactions that are required for normal craniofacial development.

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 16p12.1 deletion orthologs are expressed in motile neural crest cells and are important for regulating craniofacial development in Xenopus laevis

2020 ◽  
Author(s):  
Micaela Lasser ◽  
Jessica Bolduc ◽  
Luke Murphy ◽  
Caroline O'Brien ◽  
Sangmook Lee ◽  
...  
Keyword(s):  
Xenopus Laevis ◽  
Neural Crest ◽  
Expression Patterns ◽  
Copy Number Variants ◽  
Neural Crest Cell ◽  
Underlying Mechanism ◽  
Craniofacial Development ◽  
Pharyngeal Arches ◽  
Individual Gene ◽  
Vertebrate Model

Copy number variants (CNVs) associated with neurodevelopmental disorders are characterized by extensive phenotypic heterogeneity. In particular, one CNV was identified in a subset of children clinically diagnosed with intellectual disabilities (ID) that results in a hemizygous deletion of multiple genes at chromosome 16p12.1. In addition to ID, individuals with this deletion display a variety of symptoms including microcephaly, seizures, cardiac defects, and growth retardation. Moreover, patients also manifest severe craniofacial abnormalities, such as micrognathia, cartilage malformation of the ears and nose, and facial asymmetries; however, the function of the genes within the 16p12.1 region have not been studied in the context of vertebrate craniofacial development. The craniofacial tissues affected in patients with this deletion all derive from the same embryonic precursor, the cranial neural crest, leading to the hypothesis that one or more of the 16p12.1 genes may be involved in regulating neural crest cell (NCC)-related processes. To examine this, we characterized the developmental role of the 16p12.1-affected gene orthologs, polr3e, mosmo, uqcrc2, and cdr2, during craniofacial morphogenesis in the vertebrate model system, Xenopus laevis. While the currently-known cellular functions of these genes are diverse, we find that they share similar expression patterns along the neural tube, pharyngeal arches, and later craniofacial structures. As these genes show co-expression in the pharyngeal arches where NCCs reside, we sought to elucidate the effect of individual gene depletion on craniofacial development and NCC migration. We find that reduction of several 16p12.1 genes significantly disrupts craniofacial and cartilage formation, pharyngeal arch migration, as well as NCC specification and motility. Thus, we have determined that some of these genes play an essential role during vertebrate craniofacial patterning by regulating specific processes during NCC development, which may be an underlying mechanism contributing to the craniofacial defects associated with the 16p12.1 deletion.

scholarly journals Origins of the avian neural crest: the role of neural plate-epidermal interactions

Development ◽  
1995 ◽  
Vol 121 (2) ◽  
pp. 525-538 ◽  
Author(s):  
M.A. Selleck ◽  
M. Bronner-Fraser
Keyword(s):  
Neural Crest ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Neural Plate ◽  
Neural Tube Closure ◽  
Whole Embryo Culture ◽  
Early Stages ◽  
Tissue Interactions ◽  
Neural Ectoderm

We have investigated the lineage and tissue interactions that result in avian neural crest cell formation from the ectoderm. Presumptive neural plate was grafted adjacent to non-neural ectoderm in whole embryo culture to examine the role of tissue interactions in ontogeny of the neural crest. Our results show that juxtaposition of non-neural ectoderm and presumptive neural plate induces the formation of neural crest cells. Quail/chick recombinations demonstrate that both the prospective neural plate and the prospective epidermis can contribute to the neural crest. When similar neural plate/epidermal confrontations are performed in tissue culture to look at the formation of neural crest derivatives, juxtaposition of epidermis with either early (stages 4–5) or later (stages 6–10) neural plate results in the generation of both melanocytes and sympathoadrenal cells. Interestingly, neural plates isolated from early stages form no neural crest cells, whereas those isolated later give rise to melanocytes but not crest-derived sympathoadrenal cells. Single cell lineage analysis was performed to determine the time at which the neural crest lineage diverges from the epidermal lineage and to elucidate the timing of neural plate/epidermis interactions during normal development. Our results from stage 8 to 10+ embryos show that the neural plate/neural crest lineage segregates from the epidermis around the time of neural tube closure, suggesting that neural induction is still underway at open neural plate stages.

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

scholarly journals Neural tube-ectoderm interactions are required for trigeminal placode formation

Development ◽  
1997 ◽  
Vol 124 (21) ◽  
pp. 4287-4295 ◽  
Author(s):  
M.R. Stark ◽  
J. Sechrist ◽  
M. Bronner-Fraser ◽  
C. Marcelle
Keyword(s):  
Neural Crest ◽  
Trigeminal Ganglion ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Surface Ectoderm ◽  
Somite Stage ◽  
Tissue Interactions ◽  
Cranial Neural Crest Cells ◽  
Cranial Sensory Ganglia ◽  
Placode Formation

Cranial sensory ganglia in vertebrates develop from the ectodermal placodes, the neural crest, or both. Although much is known about the neural crest contribution to cranial ganglia, relatively little is known about how placode cells form, invaginate and migrate to their targets. Here, we identify Pax-3 as a molecular marker for placode cells that contribute to the ophthalmic branch of the trigeminal ganglion and use it, in conjunction with DiI labeling of the surface ectoderm, to analyze some of the mechanisms underlying placode development. Pax-3 expression in the ophthalmic placode is observed as early as the 4-somite stage in a narrow band of ectoderm contiguous to the midbrain neural folds. Its expression broadens to a patch of ectoderm adjacent to the midbrain and the rostral hindbrain at the 8- to 10-somite stage. Invagination of the first Pax-3-positive cells begins at the 13-somite stage. Placodal invagination continues through the 35-somite stage, by which time condensation of the trigeminal ganglion has begun. To challenge the normal tissue interactions leading to placode formation, we ablated the cranial neural crest cells or implanted barriers between the neural tube and the ectoderm. Our results demonstrate that, although the presence of neural crest cells is not mandatory for Pax-3 expression in the forming placode, a diffusible signal from the neuroectoderm is required for induction and/or maintenance of the ophthalmic placode.

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.

Patterning the vertebrate head: murine Hox 2 genes mark distinct subpopulations of premigratory and migrating cranial neural crest

Development ◽  
1991 ◽  
Vol 112 (1) ◽  
pp. 43-50 ◽  
Author(s):  
P. Hunt ◽  
D. Wilkinson ◽  
R. Krumlauf
Keyword(s):  
Neural Crest ◽  
Hox Genes ◽  
Positional Information ◽  
Branchial Arch ◽  
Neural Plate ◽  
Surface Ectoderm ◽  
Homologous Genes ◽  
The Face ◽  
Facial Pattern ◽  
Restricted Pattern

The structures of the face in vertebrates are largely derived from neural crest. There is some evidence to suggest that the form of the facial pattern is determined by the crest, and that it is specified before migration as to the structures that is is able to form. The neural crest is able to control the form of surrounding, non-neural crest tissues by an instructive interaction. Some of this cranial crest is derived from a region of the hindbrain that expresses Hox 2 homeobox genes in an overlapping and segment-restricted pattern. We have found that neurogenic and mesenchymal neural crest expresses Hox 2 genes from its point of origin beside the neural plate, during migration and after migration has ceased and that rhombomeres 3 and 5 do not have any expressing neural crest beside them. Each branchial arch expresses a different combination or code of Hox genes in a segment-restricted way. The surface ectoderm over the arches initially does not express Hox genes, and later adopts an expression pattern that reflects that of neural crest that has come to underlie it. We suggest that initially the neural plate and neural crest are spatially specified, while the surface ectoderm is unpatterned. Subsequently some positional information could be transferred to the surface ectoderm as a result of an interaction with the neural crest. Given that the role of the homologous genes in insects is position specification, and that neural crest is imprinted before migration, we suggest that Hox 2 genes are providing part of this positional information to the neural crest and hence are involved in patterning the structures of the branchial arches.

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