Avenues for Investigating the Neural Crest and Its Derivatives in Non-model (Unconventional) Vertebrates: A Craniofacial Skeleton Perspective

2019 ◽  
pp. 207-221 ◽  
Author(s):  
Michael J. Depew ◽  
Federica Bertocchini
Keyword(s):  
Neural Crest ◽  
Craniofacial Skeleton

scholarly journals Neural crest requires Impdh 2 for development of the enteric nervous system, great vessels, and craniofacial skeleton

2016 ◽  
Vol 409 (1) ◽  
pp. 152-165 ◽  
Author(s):  
Jonathan I. Lake ◽  
Marina Avetisyan ◽  
Albert G. Zimmermann ◽  
Robert O. Heuckeroth
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Enteric Nervous System ◽  
Craniofacial Skeleton ◽  
Great Vessels

scholarly journals Reactivation of the pluripotency program precedes formation of the cranial neural crest

Science ◽  
2021 ◽  
Vol 371 (6529) ◽  
pp. eabb4776 ◽  
Author(s):  
Antoine Zalc ◽  
Rahul Sinha ◽  
Gunsagar S. Gulati ◽  
Daniel J. Wesche ◽  
Patrycja Daszczuk ◽  
...  
Keyword(s):  
Neural Crest ◽  
Craniofacial Development ◽  
Open Chromatin ◽  
Cranial Neural Crest ◽  
Craniofacial Skeleton ◽  
Differentiation Potential ◽  
Subsequent Formation ◽  
Developmental Potential ◽  
Epiblast Stem Cells ◽  
Cranial Neural Crest Cells

During development, cells progress from a pluripotent state to a more restricted fate within a particular germ layer. However, cranial neural crest cells (CNCCs), a transient cell population that generates most of the craniofacial skeleton, have much broader differentiation potential than their ectodermal lineage of origin. Here, we identify a neuroepithelial precursor population characterized by expression of canonical pluripotency transcription factors that gives rise to CNCCs and is essential for craniofacial development. Pluripotency factor Oct4 is transiently reactivated in CNCCs and is required for the subsequent formation of ectomesenchyme. Furthermore, open chromatin landscapes of Oct4+ CNCC precursors resemble those of epiblast stem cells, with additional features suggestive of priming for mesenchymal programs. We propose that CNCCs expand their developmental potential through a transient reacquisition of molecular signatures of pluripotency.

scholarly journals The osteogenic potential of the neural crest lineage may contribute to craniosynostosis

2018 ◽  
Author(s):  
Daniel Doro ◽  
Annie Liu ◽  
Agamemnon E Grigoriadis ◽  
Karen J Liu
Keyword(s):  
Neural Crest ◽  
Mouse Models ◽  
Dura Mater ◽  
Osteogenic Potential ◽  
Cranial Sutures ◽  
Craniofacial Skeleton ◽  
Primary Driver ◽  
Parietal Bones ◽  
Do So

AbstractThe craniofacial skeleton is formed from the neural crest and mesodermal lineages, both of which contribute mesenchymal precursors during formation of the skull bones. The large majority of cranial sutures also include a proportion of neural crest derived mesenchyme. While some studies have addressed the relative healing abilities of neural crest and mesodermal bone, relatively little attention has been paid to differences in intrinsic osteogenic potential. Here we use mouse models to compare neural crest osteoblasts (from frontal bones or dura mater) to mesodermal osteoblasts (from parietal bones). Using in vitro culture approaches we find that neural crest-derived osteoblasts readily generate bony nodules while mesodermal osteoblasts do so less efficiently. Furthermore, we find that co-culture of neural crest-derived osteoblasts with mesodermal osteoblasts is sufficient to nucleate ossification centres. All together, this suggests that the intrinsic osteogenic abilities of neural crest-derived mesenchyme may be a primary driver behind craniosynostosis.

scholarly journals Cranial Neural Crest Cells and Their Role in the Pathogenesis of Craniofacial Anomalies and Coronal Craniosynostosis

2020 ◽  
Vol 8 (3) ◽  
pp. 18 ◽  
Author(s):  
Erica M. Siismets ◽  
Nan E. Hatch
Keyword(s):  
Neural Crest ◽  
Treatment Strategies ◽  
Neural Crest Cells ◽  
Parietal Bone ◽  
Paraxial Mesoderm ◽  
Treacher Collins Syndrome ◽  
Craniofacial Anomalies ◽  
Cranial Neural Crest ◽  
Craniofacial Skeleton ◽  
Cranial Neural Crest Cells

Craniofacial anomalies are among the most common of birth defects. The pathogenesis of craniofacial anomalies frequently involves defects in the migration, proliferation, and fate of neural crest cells destined for the craniofacial skeleton. Genetic mutations causing deficient cranial neural crest migration and proliferation can result in Treacher Collins syndrome, Pierre Robin sequence, and cleft palate. Defects in post-migratory neural crest cells can result in pre- or post-ossification defects in the developing craniofacial skeleton and craniosynostosis (premature fusion of cranial bones/cranial sutures). The coronal suture is the most frequently fused suture in craniosynostosis syndromes. It exists as a biological boundary between the neural crest-derived frontal bone and paraxial mesoderm-derived parietal bone. The objective of this review is to frame our current understanding of neural crest cells in craniofacial development, craniofacial anomalies, and the pathogenesis of coronal craniosynostosis. We will also discuss novel approaches for advancing our knowledge and developing prevention and/or treatment strategies for craniofacial tissue regeneration and craniosynostosis.

The zebrafish colourless gene regulates development of non-ectomesenchymal neural crest derivatives

Development ◽  
2000 ◽  
Vol 127 (3) ◽  
pp. 515-525 ◽  
Author(s):  
R.N. Kelsh ◽  
J.S. Eisen
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Cell Types ◽  
Pigment Cells ◽  
Specific Cell ◽  
Zebrafish Embryos ◽  
Craniofacial Skeleton ◽  
Cell Fates ◽  
Peripheral Neurons ◽  
Neural Crest Development

Neural crest forms four major categories of derivatives: pigment cells, peripheral neurons, peripheral glia, and ectomesenchymal cells. Some early neural crest cells generate progeny of several fates. How specific cell fates become specified is still poorly understood. Here we show that zebrafish embryos with mutations in the colourless gene have severe defects in most crest-derived cell types, including pigment cells, neurons and specific glia. In contrast, craniofacial skeleton and medial fin mesenchyme are normal. These observations suggest that colourless has a key role in development of non-ectomesenchymal neural crest fates, but not in development of ectomesenchymal fates. Thus, the cls mutant phenotype reveals a segregation of ectomesenchymal and non-ectomesenchymal fates during zebrafish neural crest development. The combination of pigmentation and enteric nervous system defects makes colourless mutations a model for two human neurocristopathies, Waardenburg-Shah syndrome and Hirschsprung's disease.

scholarly journals GATA4 as a novel regulator involved in the development of the neural crest and craniofacial skeleton via Barx1

2018 ◽  
Vol 25 (11) ◽  
pp. 1996-2009 ◽  
Author(s):  
Shuyu Guo ◽  
Yuxin Zhang ◽  
Tingting Zhou ◽  
Dongyue Wang ◽  
Yajuan Weng ◽  
...  
Keyword(s):  
Neural Crest ◽  
Craniofacial Skeleton

scholarly journals Kat2a and Kat2b Acetyltransferase Activity Regulates Craniofacial Cartilage and Bone Differentiation in Zebrafish and Mice

2018 ◽  
Vol 6 (4) ◽  
pp. 27 ◽  
Author(s):  
Rwik Sen ◽  
Sofia Pezoa ◽  
Lomeli Carpio Shull ◽  
Laura Hernandez-Lagunas ◽  
Lee Niswander ◽  
...  
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Cellular Growth ◽  
Cranial Neural Crest ◽  
Craniofacial Skeleton ◽  
Altered Expression ◽  
Precise Control ◽  
H3k9 Acetylation ◽  
Cranial Neural Crest Cells ◽  
And Cartilage

Cranial neural crest cells undergo cellular growth, patterning, and differentiation within the branchial arches to form cartilage and bone, resulting in a precise pattern of skeletal elements forming the craniofacial skeleton. However, it is unclear how cranial neural crest cells are regulated to give rise to the different shapes and sizes of the bone and cartilage. Epigenetic regulators are good candidates to be involved in this regulation, since they can exert both broad as well as precise control on pattern formation. Here, we investigated the role of the histone acetyltransferases Kat2a and Kat2b in craniofacial development using TALEN/CRISPR/Cas9 mutagenesis in zebrafish and the Kat2ahat/hat (also called Gcn5) allele in mice. kat2a and kat2b are broadly expressed during embryogenesis within the central nervous system and craniofacial region. Single and double kat2a and kat2b zebrafish mutants have an overall shortening and hypoplastic nature of the cartilage elements and disruption of the posterior ceratobranchial cartilages, likely due to smaller domains of expression of both cartilage- and bone-specific markers, including sox9a and col2a1, and runx2a and runx2b, respectively. Similarly, in mice we observe defects in the craniofacial skeleton, including hypoplastic bone and cartilage and altered expression of Runx2 and cartilage markers (Sox9, Col2a1). In addition, we determined that following the loss of Kat2a activity, overall histone 3 lysine 9 (H3K9) acetylation, the main epigenetic target of Kat2a/Kat2b, was decreased. These results suggest that Kat2a and Kat2b are required for growth and differentiation of craniofacial cartilage and bone in both zebrafish and mice by regulating H3K9 acetylation.

Compensatory defects associated with mutations in Hoxa1 restore normal palatogenesis to Hoxa2 mutants

Development ◽  
1999 ◽  
Vol 126 (22) ◽  
pp. 5011-5026 ◽  
Author(s):  
J.R. Barrow ◽  
M.R. Capecchi
Keyword(s):  
Cleft Palate ◽  
Neural Crest ◽  
Craniofacial Development ◽  
Sensory Ganglia ◽  
Craniofacial Skeleton ◽  
Multiple Defects ◽  
Abnormal Posture ◽  
Gene Functions ◽  
Craniofacial Defects ◽  
Cranial Sensory Ganglia

The rhombencephalic neural crest play several roles in craniofacial development. They give rise to the cranial sensory ganglia and much of the craniofacial skeleton, and are vital for patterning of the craniofacial muscles. The loss of Hoxa1 or Hoxa2 function affects the development of multiple neural crest-derived structures. To understand how these two genes function together in craniofacial development, an allele was generated that disrupts both of these linked genes. Some of the craniofacial defects observed in the double mutants were additive combinations of those that exist in each of the single mutants, indicating that each gene functions independently in the formation of these structures. Other defects were found only in the double mutants demonstrating overlapping or synergistic functions. We also uncovered multiple defects in the attachments and trajectories of the extrinsic tongue and hyoid muscles in Hoxa2 mutants. Interestingly, the abnormal trajectory of two of these muscles, the styloglossus and the stylohyoideus, blocked the attachment of the hyoglossus to the greater horn of the hyoid, which in turn correlated exactly with the presence of cleft palate in Hoxa2 mutants. We suggest that the hyoglossus, whose function is to depress the lateral edges of the tongue, when unable to make its proper attachment to the greater horn of the hyoid, forces the tongue to adopt an abnormal posture which blocks closure of the palatal shelves. Unexpectedly, in Hoxa1/Hoxa2 double mutants, the penetrance of cleft palate is dramatically reduced. We show that two compensatory defects, associated with the loss of Hoxa1 function, restore normal attachment of the hyoglossus to the greater horn thereby allowing the palatal shelves to lift and fuse above the flattened tongue.

Sign in / Sign up

Export Citation Format

Share Document