The transcription factor Sox9 is required for cranial neural crest development inXenopus

Development ◽  
2002 ◽  
Vol 129 (2) ◽  
pp. 421-432 ◽  
Author(s):  
Rebecca F. Spokony ◽  
Yoichiro Aoki ◽  
Natasha Saint-Germain ◽  
Emily Magner-Fink ◽  
Jean-Pierre Saint-Jeannet
Keyword(s):  
Neural Crest ◽  
Cell Fate ◽  
Neural Plate ◽  
Cranial Neural Crest ◽  
Pharyngeal Arches ◽  
Skeletal Malformations ◽  
Xy Sex Reversal ◽  
Human Disorder ◽  
Antisense Oligos ◽  
Craniofacial Defects

The SOX family of transcription factors has been implicated in cell fate specification during embryogenesis. One member of this family, Sox9, has been shown to regulate both chondrogenesis and sex determination in the mouse embryo. Heterozygous mutations in Sox9 result in Campomelic Dysplasia (CD), a lethal human disorder characterized by autosomal XY sex reversal, severe skeletal malformations and several craniofacial defects. Sox9 is also expressed in neural crest progenitors but very little is known about the function of Sox9 in the neural crest. We have cloned the Xenopus homolog of the Sox9 gene. It is expressed maternally and accumulates shortly after gastrulation at the lateral edges of the neural plate, in the neural crest-forming region. As development proceeds, Sox9 expression persists in migrating cranial crest cells as they populate the pharyngeal arches. Depletion of Sox9 protein in developing embryos, using morpholino antisense oligos, causes a dramatic loss of neural crest progenitors and an expansion of the neural plate. Later during embryogenesis, morpholino-treated embryos have a specific loss or reduction of neural crest-derived skeletal elements, mimicking one aspect of the craniofacial defects observed in CD patients. We propose that Sox9 is an essential component of the regulatory pathway that leads to cranial neural crest formation.

Early Craniofacial Defects in Zebrafish that Have Reduced Function of a Wnt-Interacting Extracellular Matrix Protein, Tinagl1

2017 ◽  
Vol 54 (4) ◽  
pp. 381-390 ◽  
Author(s):  
Hannah Neiswender ◽  
Sammy Navarre ◽  
David J. Kozlowski ◽  
Ellen K. Lemosy
Keyword(s):  
Neural Crest ◽  
Cleft Lip ◽  
Matrix Protein ◽  
Bone Development ◽  
Neural Crest Cells ◽  
Extracellular Matrix Protein ◽  
Cranial Neural Crest ◽  
Pharyngeal Arches ◽  
Cranial Neural Crest Cells ◽  
Craniofacial Defects

Objective Tinagl1 has a weak genetic association with craniosynostosis, but its functions in cartilage and bone development are unknown. Knockdown of Tinagl1 in zebrafish embryos allowed an initial characterization of its potential effects on craniofacial cartilage development and a test of whether these effects could involve Wnt signaling. Results Tinagl1 knockdown resulted in dose-dependent reductions and defects in ventral pharyngeal arch cartilages as well as the ethmoid plate, a zebrafish correlate to the palate. These defects could be correlated to reduced numbers of cranial neural crest cells in the pharyngeal arches and could be reproduced with comanipulation of Tinagl1 and Wnt3a by morpholino-based knockdown. Conclusions These results suggest that Tinagl1 is required early in the proliferation or migration of cranial neural crest cells and that its effects are mediated via Wnt3a signaling. Because Wnt3a is among the Wnts that contribute to nonsyndromic cleft lip and cleft palate in mouse and man, further investigation of Tinagl1 may help to elucidate mechanisms underlying these disorders.

Regulation of cranial neural crest cell fate by Irf6 and Twist1 interaction

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Walid D. Fakhouri ◽  
Jessica Wildgrube Bertol ◽  
Victoria K. Xie ◽  
Shelby Johnston ◽  
Kelsea Hubka ◽  
...  
Keyword(s):  
Neural Crest ◽  
Cell Fate ◽  
Neural Crest Cell ◽  
Cranial Neural Crest ◽  
Cranial Neural Crest Cell ◽  
Crest Cell

scholarly journals Lifelong single-cell profiling of cranial neural crest diversification

2021 ◽  
Author(s):  
Peter Fabian ◽  
Kuo-Chang Tseng ◽  
Mathi Thiruppathy ◽  
Claire Arata ◽  
Hung-Jhen Chen ◽  
...  
Keyword(s):  
Neural Crest ◽  
Single Cell ◽  
Cell Fate ◽  
Intrinsic Property ◽  
Chromatin Accessibility ◽  
Specific Cell ◽  
List Type ◽  
Cranial Neural Crest ◽  
Cell Transcriptome ◽  
Single Cell Transcriptome

AbstractThe cranial neural crest generates a huge diversity of derivatives, including the bulk of connective and skeletal tissues of the vertebrate head. How neural crest cells acquire such extraordinary lineage potential remains unresolved. By integrating single-cell transcriptome and chromatin accessibility profiles of cranial neural crest-derived cells across the zebrafish lifetime, we observe region-specific establishment of enhancer accessibility for distinct fates. Neural crest-derived cells rapidly diversify into specialized progenitors, including multipotent skeletal progenitors, stromal cells with a regenerative signature, fibroblasts with a unique metabolic signature linked to skeletal integrity, and gill-specific progenitors generating cell types for respiration. By retrogradely mapping the emergence of lineage-specific chromatin accessibility, we identify a wealth of candidate lineage-priming factors, including a Gata3 regulatory circuit for respiratory cell fates. Rather than multilineage potential being an intrinsic property of cranial neural crest, our findings support progressive and region-specific chromatin remodeling underlying acquisition of diverse neural crest lineage potential.HighlightsSingle-cell transcriptome and chromatin atlas of cranial neural crestProgressive emergence of region-specific cell fate competencyChromatin accessibility mapping identifies candidate lineage regulatorsGata3 function linked to gill-specific respiratory programGraphical Abstract

scholarly journals PFKFB4 control of Akt signaling is essential for premigratory and migratory neural crest formation

2017 ◽  
Author(s):  
Ana Leonor Figueiredo ◽  
Frédérique Maczkowiak ◽  
Caroline Borday ◽  
Patrick Pla ◽  
Meghane Sittewelle ◽  
...  
Keyword(s):  
Neural Crest ◽  
Early Phase ◽  
Akt Signaling ◽  
Neural Plate ◽  
Summary Statement ◽  
And Migration ◽  
Craniofacial Defects ◽  
Later Phase ◽  
Adult Cells

Summary statementPFKFB4 controls neural crest final specification and migration by regulation of AKT signaling or glycolysis.AbstractNeural crest (NC) specification comprises an early phase, initiating immature NC progenitors formation at neural plate stage, and a later phase at neural fold stage, resulting into functional premigratory NC, able to delaminate and migrate. We found that the NC-GRN triggers up-regulation of pfkfb4 (6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 4) during this late specification phase. As shown in previous studies, PFKFB4 controls AKT signaling in gastrulas and glycolysis rate in adult cells. Here, we focus on PFKFB4 function in NC during and after neurulation, using time-controlled or hypomorph depletions in vivo. We find that PFKFB4 is essential both for specification of functional premigratory NC and for its migration. PFKFB4-depleted embryos fail activating n-cadherin and late NC specifiers, exhibit severe migration defects, resulting in craniofacial defects. AKT signaling mediates PFKFB4 function in NC late specification, while both AKT signaling and glycolysis regulate migration. These findings highlight novel and critical roles of PFKFB4 activity in later stages of NC development, wired into the NC-GRN.

Delta signaling mediates segregation of neural crest and spinal sensory neurons from zebrafish lateral neural plate

Development ◽  
2000 ◽  
Vol 127 (13) ◽  
pp. 2873-2882 ◽  
Author(s):  
R.A. Cornell ◽  
J.S. Eisen
Keyword(s):  
Neural Crest ◽  
Point Mutation ◽  
Sensory Neurons ◽  
Genetic Difference ◽  
Neural Plate ◽  
Cranial Neural Crest ◽  
Neural Crest Development ◽  
Neural Crest Derivative ◽  
Trunk Neural Crest

We examined the role of Delta signaling in specification of two derivatives in zebrafish neural plate: Rohon-Beard spinal sensory neurons and neural crest. deltaA-expressing Rohon-Beard neurons are intermingled with premigratory neural crest cells in the trunk lateral neural plate. Embryos homozygous for a point mutation in deltaA, or with experimentally reduced delta signalling, have supernumerary Rohon-Beard neurons, reduced trunk-level expression of neural crest markers and lack trunk neural crest derivatives. Fin mesenchyme, a putative trunk neural crest derivative, is present in deltaA mutants, suggesting it segregates from other neural crest derivatives as early as the neural plate stage. Cranial neural crest derivatives are also present in deltaA mutants, revealing a genetic difference in regulation of trunk and cranial neural crest development.

scholarly journals Stage-Dependent Differential Gene Expression Profiles of Cranial Neural Crest Cells Derived from Mouse Induced Pluripotent Stem Cells

2018 ◽  
Author(s):  
Ayano Odashima ◽  
Shoko Onodera ◽  
Akiko Saito ◽  
Takashi Nakamura ◽  
Yuuki Ogihara ◽  
...  
Keyword(s):  
Gene Expression ◽  
Neural Crest ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Neural Crest Cells ◽  
Cranial Neural Crest ◽  
Pharyngeal Arches ◽  
A Disintegrin And Metalloproteinase ◽  
Induced Pluripotent ◽  
Cranial Neural Crest Cells

AbstractCranial neural crest cells (cNCCs) comprise a multipotent population of cells that migrate into the pharyngeal arches of the vertebrate embryo and differentiate into a broad range of derivatives of the craniofacial organs. Consequently, migrating cNCCs are considered as one of the most attractive candidate sources of cells for regenerative medicine. In this study, we analyzed the gene expression profiles of cNCCs at different time points after induction by conducting three independent RNA sequencing experiments. We successfully induced cNCC formation from mouse induced pluripotent stem (miPS) cells by culturing them in neural crest inducing media for 14 days. We found that these cNCCs expressed several neural crest specifier genes but were lacking some previously reported specifiers, such as paired box 3 (Pax3), msh homeobox 1 (Msx1), and Forkhead box D3 (FoxD3), which are presumed to be essential for neural crest development in the embryo. Thus, a distinct molecular network may the control gene expression in miPS-derived cNCCs. We also found that c-Myc, ETS proto-oncogene 1, transcription factor (Ets1), and sex determining region Y-box 10 (Sox10) were only detected at 14 days after induction. Therefore, we assume that these genes would be useful markers for migratory cNCCs induced from miPS cells. Eventually, these cNCCs comprised a broad spectrum of protocadherin (Pcdh) and a disintegrin and metalloproteinase with thrombospondin motifs (Adamts) family proteins, which may be crucial in their migration.

scholarly journals Modulation of β-catenin levels is critical for cranial neural crest patterning and dispersal into first pharyngeal arch

2019 ◽  
Author(s):  
Alok Javali ◽  
Vairavan Laxmanan ◽  
Dasaradhi Palakodeti ◽  
Ramkumar Sambasivan
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Mouse Embryos ◽  
Pharyngeal Arch ◽  
Cranial Neural Crest ◽  
Connective Tissues ◽  
Pharyngeal Arches ◽  
Cell Arrangement ◽  
Cranial Neural Crest Cells

AbstractVertebrate cranial neural crest cells (CNCC) are multipotent. Proximal to the source CNCC form the cranial ganglia. Distally, in the pharyngeal arches, they give rise to the craniofacial skeleton and connective tissues. Fate choices are made as CNCC pattern into distinct destination compartments. In spite of this importance, the mechanism patterning CNCC is poorly defined. Here, we report that a novel β-catenin-controlled switch in the cell arrangement is critical in patterning CNCC. In mouse embryos, at the first pharyngeal arch axial level, membrane β-catenin levels correlate with the extent of cell-cell adhesion and thus, with a collective or a dispersed state of CNCC. Using in vitro human neural crest model and chemical modulators of β-catenin levels, we show a requirement for down-modulating β-catenin for the collective-to-dispersed switch. Similarly, in β-catenin gain of function mutant mouse embryos, CNCC fail to disperse, which may underlie their failure to populate first pharyngeal arch. Thus, we show that β-catenin-mediated regulation of CNCC tissue architecture, a previously underappreciated mechanism, underlies the patterning of CNCC into fate-specific compartments.Summary statementThe report shows a crucial step in cranial neural crest patterning. Neural crest cells invading the pharyngeal arches transition from a collective to a dispersed state. This transition in cell arrangement is dependent on membrane β-catenin levels.

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