A novel spalt gene expressed in branchial arches affects the ability of cranial neural crest cells to populate sensory ganglia

Cranial neural crest cells differentiate into diverse derivatives including neurons and glia of the cranial ganglia, and cartilage and bone of the facial skeleton. Here, we explore the function of a novel transcription factor of the spalt family that might be involved in early cell-lineage decisions of the avian neural crest. The chicken spalt4 gene (csal4) is expressed in the neural tube, migrating neural crest, branchial arches and, transiently, in the cranial ectoderm. Later, it is expressed in the mesectodermal, but not neuronal or glial, derivatives of midbrain and hindbrain neural crest. After over-expression by electroporation into the cranial neural tube and neural crest, we observed a marked redistribution of electroporated neural crest cells in the vicinity of the trigeminal ganglion. In control-electroporated embryos, numerous, labeled neural crest cells (∼80% of the population) entered the ganglion, many of which differentiated into neurons. By contrast, few (∼30% of the population) spalt-electroporated neural crest cells entered the trigeminal ganglion. Instead, they localized in the mesenchyme around the ganglionic periphery or continued further ventrally to the branchial arches. Interestingly, little or no expression of differentiation markers for neurons or other cell types was observed in spalt-electroporated neural crest cells.

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Twist Function Is Required for the Morphogenesis of the Cephalic Neural Tube and the Differentiation of the Cranial Neural Crest Cells in the Mouse Embryo

Developmental Biology ◽

10.1006/dbio.2002.0699 ◽

2002 ◽

Vol 247 (2) ◽

pp. 251-270 ◽

Cited By ~ 146

Author(s):

Kenneth Soo ◽

Meredith P. O'Rourke ◽

Poh-Lynn Khoo ◽

Kirsten A. Steiner ◽

Nicole Wong ◽

...

Keyword(s):

Neural Crest ◽

Neural Tube ◽

Mouse Embryo ◽

Neural Crest Cells ◽

Cranial Neural Crest ◽

Cranial Neural Crest Cells

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Neural tube-ectoderm interactions are required for trigeminal placode formation

Development ◽

10.1242/dev.124.21.4287 ◽

1997 ◽

Vol 124 (21) ◽

pp. 4287-4295 ◽

Cited By ~ 7

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.

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Effects of Retinoic Acid on the Development of the Facial Skeleton in Hamsters: Early Changes Involving Cranial Neural Crest Cells

Cells Tissues Organs ◽

10.1159/000145741 ◽

1983 ◽

Vol 116 (2) ◽

pp. 180-192 ◽

Cited By ~ 71

Author(s):

M.J. Wiley ◽

P. Cauwenbergs ◽

I.M. Taylor

Keyword(s):

Retinoic Acid ◽

Neural Crest ◽

Neural Crest Cells ◽

Cranial Neural Crest ◽

Facial Skeleton ◽

Cranial Neural Crest Cells

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TWIST1 interacts with adherens junction proteins during neural tube formation and regulates fate transition in cranial neural crest cells

10.1101/2021.08.22.457283 ◽

2021 ◽

Author(s):

Jessica W Bertol ◽

Shelby Johnston ◽

Rabia Ahmed ◽

Victoria K Xie ◽

Lissette Cruz ◽

...

Keyword(s):

Neural Crest ◽

Cell Fate ◽

Neural Tube ◽

Target Genes ◽

Structural Integrity ◽

Neural Crest Cells ◽

Neural Tube Closure ◽

Cranial Neural Crest ◽

Mesenchymal Transition ◽

Cranial Neural Crest Cells

Cell fate determination is a necessary and tightly regulated process for producing different cell types and structures during development. Cranial neural crest cells (CNCCs) are unique to vertebrate embryos and emerge from the neural fold borders into multiple cell lineages that differentiate into bone, cartilage, neurons, and glial cells. We previously reported that Irf6 genetically interacts with Twist1 during CNCC-derived tissue formation. Here, we investigated the mechanistic role of Twist1 and Irf6 at early stages of craniofacial development. Our data indicates that TWIST1 interacts with a/b/g-CATENINS during neural tube closure, and Irf6 is involved in the structural integrity of the neural tube. Twist1 suppresses Irf6 and other epithelial genes in CNCCs during epithelial-to-mesenchymal transition (EMT) process and cell migration. Conversely, a loss of Twist1 leads to a sustained expression of epithelial and cell adhesion markers in migratory CNCCs. Disruption of TWIST1 phosphorylation in vivo leads to epidermal blebbing, edema, neural tube defects, and CNCC-derived structural abnormalities. Altogether, this study describes an uncharacterized function of Twist1 and Irf6 in the neural tube and CNCCs and provides new target genes of Twist1 involved in cytoskeletal remodeling. Furthermore, the association between DNA variations within TWIST1 putative enhancers and human facial morphology is also investigated.

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Analysis of cranial neural crest migratory pathways in axolotl using cell markers and transplantation

Development ◽

10.1242/dev.127.12.2751 ◽

2000 ◽

Vol 127 (12) ◽

pp. 2751-2761 ◽

Cited By ~ 1

Author(s):

H. Epperlein ◽

D. Meulemans ◽

M. Bronner-Fraser ◽

H. Steinbeisser ◽

M.A. Selleck

Keyword(s):

Transcription Factor ◽

Neural Crest ◽

Neural Crest Cells ◽

Branchial Arch ◽

Cranial Neural Crest ◽

Branchial Arches ◽

Trunk Neural Crest ◽

Cranial Neural Crest Cells ◽

Random Nature

We have examined the ability of normal and heterotopically transplanted neural crest cells to migrate along cranial neural crest pathways in the axolotl using focal DiI injections and in situ hybridization with the neural crest marker, AP-2. DiI labeling demonstrates that cranial neural crest cells migrate as distinct streams along prescribed pathways to populate the maxillary and mandibular processes of the first branchial arch, the hyoid arch and gill arches 1–4, following migratory pathways similar to those observed in other vertebrates. Another neural crest marker, the transcription factor AP-2, is expressed by premigratory neural crest cells within the neural folds and migrating neural crest cells en route to and within the branchial arches. Rotations of the cranial neural folds suggest that premigratory neural crest cells are not committed to a specific branchial arch fate, but can compensate when displaced short distances from their targets by migrating to a new target arch. In contrast, when cells are displaced far from their original location, they appear unable to respond appropriately to their new milieu such that they fail to migrate or appear to migrate randomly. When trunk neural folds are grafted heterotopically into the head, trunk neural crest cells migrate in a highly disorganized fashion and fail to follow normal cranial neural crest pathways. Importantly, we find incorporation of some trunk cells into branchial arch cartilage despite the random nature of their migration. This is the first demonstration that trunk neural crest cells can form cartilage when transplanted to the head. Our results indicate that, although cranial and trunk neural crest cells have inherent differences in ability to recognize migratory pathways, trunk neural crest can differentiate into cranial cartilage when given proper instructive cues.

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