scholarly journals FGF and retinoic acid activity gradients control the timing of neural crest cell emigration in the trunk

2011 ◽  
Vol 194 (3) ◽  
pp. 489-503 ◽  
Author(s):  
Patricia L. Martínez-Morales ◽  
Ruth Diez del Corral ◽  
Isabel Olivera-Martínez ◽  
Alejandra C. Quiroga ◽  
Raman M. Das ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Neural Crest ◽  
Epithelial Mesenchymal Transition ◽  
Neural Crest Cell ◽  
Fibroblast Growth ◽  
Loss Of Function ◽  
Mesenchymal Transition ◽  
Morphogenetic Protein ◽  
Trunk Neural Crest ◽  
Crest Cell

Coordination between functionally related adjacent tissues is essential during development. For example, formation of trunk neural crest cells (NCCs) is highly influenced by the adjacent mesoderm, but the molecular mechanism involved is not well understood. As part of this mechanism, fibroblast growth factor (FGF) and retinoic acid (RA) mesodermal gradients control the onset of neurogenesis in the extending neural tube. In this paper, using gain- and loss-of-function experiments, we show that caudal FGF signaling prevents premature specification of NCCs and, consequently, premature epithelial–mesenchymal transition (EMT) to allow cell emigration. In contrast, rostrally generated RA promotes EMT of NCCs at somitic levels. Furthermore, we show that FGF and RA signaling control EMT in part through the modulation of elements of the bone morphogenetic protein and Wnt signaling pathways. These data establish a clear role for opposition of FGF and RA signaling in control of the timing of NCC EMT and emigration and, consequently, coordination of the development of the central and peripheral nervous system during vertebrate trunk elongation.

scholarly journals p53 coordinates cranial neural crest cell growth and epithelial-mesenchymal transition/delamination processes

Development ◽  
2011 ◽  
Vol 138 (9) ◽  
pp. 1827-1838 ◽  
Author(s):  
A. Rinon ◽  
A. Molchadsky ◽  
E. Nathan ◽  
G. Yovel ◽  
V. Rotter ◽  
...  
Keyword(s):  
Cell Growth ◽  
Neural Crest ◽  
Epithelial Mesenchymal Transition ◽  
Neural Crest Cell ◽  
Cranial Neural Crest ◽  
Mesenchymal Transition ◽  
Cranial Neural Crest Cell ◽  
Crest Cell

scholarly journals Establishment of a murine culture system for modeling the temporal progression of cranial and trunk neural crest cell differentiation

2018 ◽  
Vol 11 (12) ◽  
pp. dmm035097 ◽  
Author(s):  
Maria R. Replogle ◽  
Virinchipuram S. Sreevidya ◽  
Vivian M. Lee ◽  
Michael D. Laiosa ◽  
Kurt R. Svoboda ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Neural Crest ◽  
Culture System ◽  
Neural Crest Cell ◽  
Trunk Neural Crest ◽  
Crest Cell

scholarly journals Crucial and Overlapping Roles of Six1 and Six2 in Craniofacial Development

2019 ◽  
Vol 98 (5) ◽  
pp. 572-579 ◽  
Author(s):  
Z. Liu ◽  
C. Li ◽  
J. Xu ◽  
Y. Lan ◽  
H. Liu ◽  
...  
Keyword(s):  
Neural Crest ◽  
Ectopic Expression ◽  
Mandibular Condyle ◽  
Neural Crest Cell ◽  
Messenger Rnas ◽  
Developmental Defects ◽  
Facial Cleft ◽  
Frontonasal Dysplasia ◽  
Morphogenetic Protein ◽  
Crest Cell

SIX1 and SIX2 encode closely related transcription factors of which disruptions have been associated with distinct craniofacial syndromes, with mutations in SIX1 associated with branchiootic syndrome 3 (BOS3) and heterozygous deletions of SIX2 associated with frontonasal dysplasia defects. Whereas mice deficient in Six1 recapitulated most of the developmental defects associated with BOS3, mice lacking Six2 function had no obvious frontonasal defects. We show that Six1 and Six2 exhibit partly overlapping patterns of expression in the developing mouse embryonic frontonasal, maxillary, and mandibular processes. We found that Six1 –/– Six2 –/– double-mutant mice were born with severe craniofacial deformity not seen in the Six1 –/– or Six2 –/– single mutants, including skull bone agenesis, midline facial cleft, and syngnathia. Moreover, whereas Six1 –/– mice exhibited partial transformation of maxillary zygomatic bone into a mandibular condyle-like structure, Six1 –/–Six2 +/– mice exhibit significantly increased penetrance of the maxillary malformation. In addition to ectopic Dlx5 expression at the maxillary-mandibular junction as recently reported in E10.5 Six1 –/– embryos, the E10.5 Six1 –/– Six2 +/– embryos showed ectopic expression of Bmp4, Msx1, and Msx2 messenger RNAs in the maxillary-mandibular junction. Genetically inactivating 1 allele of either Ednra or Bmp4 significantly reduced the penetrance of maxillary malformation in both Six1 –/– and Six1 –/– Six2 +/– embryos, indicating that Six1 and Six2 regulate both endothelin and bone morphogenetic protein-4 signaling pathways to pattern the facial structures. Furthermore, we show that neural crest–specific inactivation of Six1 in Six2 –/– embryos resulted in midline facial cleft and frontal bone agenesis. We show that Six1 –/– Six2 –/– embryos exhibit significantly reduced expression of key frontonasal development genes Alx1 and Alx3 as well as increased apoptosis in the developing frontonasal mesenchyme. Together, these results indicate that Six1 and Six2 function partly redundantly to control multiple craniofacial developmental processes and play a crucial neural crest cell–autonomous role in frontonasal morphogenesis.

scholarly journals A chemotactic model of trunk neural crest cell migration

genesis ◽  
2018 ◽  
Vol 56 (9) ◽  
pp. e23239 ◽  
Author(s):  
Louise Dyson ◽  
Alexander Holmes ◽  
Ang Li ◽  
Paul M. Kulesa
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Neural Crest Cell Migration ◽  
Trunk Neural Crest ◽  
Crest Cell

scholarly journals Connexin 43 impacts the chick premigratory cranial neural crest cell population without affecting the neural crest cell epithelial-to-mesenchymal transition

2019 ◽  
Author(s):  
Karyn Jourdeuil ◽  
Lisa A. Taneyhill
Keyword(s):  
Gap Junctions ◽  
Neural Crest ◽  
Gap Junction ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Cranial Neural Crest ◽  
Mesenchymal Transition ◽  
Junction Protein ◽  
Cranial Neural Crest Cells ◽  
Crest Cell

ABSTRACTGap junctions are intercellular channels that allow for the diffusion of small ions and solutes between coupled cells. Connexin 43 (Cx43), also known as Gap Junction Protein α1, is the most broadly expressed gap junction protein in vertebrate development. Cx43 is strongly expressed in premigratory cranial neural crest cells and is maintained throughout the neural crest cell epithelial-to-mesenchymal transition (EMT), but its function in these cells is not known. To this end, we have used a combination of in vivo and ex vivo live imaging with confocal microscopy, immunohistochemistry, and functional assays to assess gap junction formation, and Cx43 function, in chick premigratory cranial neural crest cells. Our results demonstrate that gap junctions exist between chick premigratory and migratory cranial neural crest cells, with Cx43 depletion inhibiting the function of gap junctions. While a reduction in Cx43 levels just prior to neural crest cell EMT did not affect EMT and subsequent emigration of neural crest cells from the neural tube, the size of the premigratory neural crest cell domain was decreased in the absence of any changes in cell proliferation or death. Collectively, these data identify a role for Cx43 within the chick premigratory cranial neural crest cell population prior to EMT and migration.

Sign in / Sign up

Export Citation Format

Share Document