The chinless mutation and neural crest cell interactions in zebrafish jaw development

Development ◽  
1996 ◽  
Vol 122 (5) ◽  
pp. 1417-1426 ◽  
Author(s):  
T.F. Schilling ◽  
C. Walker ◽  
C.B. Kimmel
Keyword(s):  
Neural Crest ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Paraxial Mesoderm ◽  
Wild Type ◽  
Host Genotype ◽  
Pharyngeal Arches ◽  
Expression Studies ◽  
Gene Expression Studies ◽  
Cranial Neural Crest Cells

During vertebrate development, neural crest cells are thought to pattern many aspects of head organization, including the segmented skeleton and musculature of the jaw and gills. Here we describe mutations at the gene chinless, chn, that disrupt the skeletal fates of neural crest cells in the head of the zebrafish and their interactions with muscle precursors. chn mutants lack neural-crest-derived cartilage and mesoderm-derived muscles in all seven pharyngeal arches. Fate mapping and gene expression studies demonstrate the presence of both undifferentiated cartilage and muscle precursors in mutants. However, chn blocks differentiation directly in neural crest, and not in mesoderm, as revealed by mosaic analyses. Neural crest cells taken from wild-type donor embryos can form cartilage when transplanted into chn mutant hosts and rescue some of the patterning defects of mutant pharyngeal arches. In these cases, cartilage only forms if neural crest is transplanted at least one hour before its migration, suggesting that interactions occur transiently in early jaw precursors. In contrast, transplanted cells in paraxial mesoderm behave according to the host genotype; mutant cells form jaw muscles in a wild-type environment. These results suggest that chn is required for the development of pharyngeal cartilages from cranial neural crest cells and subsequent crest signals that pattern mesodermally derived myocytes.

sucker encodes a zebrafish Endothelin-1 required for ventral pharyngeal arch development

Development ◽  
2000 ◽  
Vol 127 (17) ◽  
pp. 3815-3828 ◽  
Author(s):  
C.T. Miller ◽  
T.F. Schilling ◽  
K. Lee ◽  
J. Parker ◽  
C.B. Kimmel
Keyword(s):  
Neural Crest ◽  
Expression Patterns ◽  
Neural Crest Cells ◽  
Paraxial Mesoderm ◽  
Dorsoventral Patterning ◽  
Surface Ectoderm ◽  
Pharyngeal Arches ◽  
Endothelin 1 ◽  
Lower Jaw ◽  
Arch Neural

Mutation of sucker (suc) disrupts development of the lower jaw and other ventral cartilages in pharyngeal segments of the zebrafish head. Our sequencing, cosegregation and rescue results indicate that suc encodes an Endothelin-1 (Et-1). Like mouse and chick Et-1, suc/et-1 is expressed in a central core of arch paraxial mesoderm and in arch epithelia, both surface ectoderm and pharyngeal endoderm, but not in skeletogenic neural crest. Long before chondrogenesis, suc/et-1 mutant embryos have severe defects in ventral arch neural crest expression of dHAND, dlx2, msxE, gsc, dlx3 and EphA3 in the anterior arches. Dorsal expression patterns are unaffected. Later in development, suc/et-1 mutant embryos display defects in mesodermal and endodermal tissues of the pharynx. Ventral premyogenic condensations fail to express myoD, which correlates with a ventral muscle defect. Further, expression of shh in endoderm of the first pharyngeal pouch fails to extend as far laterally as in wild types. We use mosaic analyses to show that suc/et-1 functions nonautonomously in neural crest cells, and is thus required in the environment of postmigratory neural crest cells to specify ventral arch fates. Our mosaic analyses further show that suc/et-1 nonautonomously functions in mesendoderm for ventral arch muscle formation. Collectively our results support a model for dorsoventral patterning of the gnathostome pharyngeal arches in which Et-1 in the environment of the postmigratory cranial neural crest specifies the lower jaw and other ventral arch fates.

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.

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.

scholarly journals The alx3 gene shapes the zebrafish neurocranium by regulating frontonasal neural crest cell differentiation timing

Development ◽  
2021 ◽  
Vol 148 (7) ◽  
Author(s):  
Jennyfer M. Mitchell ◽  
Juliana Sucharov ◽  
Anthony T. Pulvino ◽  
Elliott P. Brooks ◽  
Austin E. Gillen ◽  
...  
Keyword(s):  
Neural Crest ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Developmental Timing ◽  
Cranial Neural Crest ◽  
Different Populations ◽  
Cell Subpopulations ◽  
Cranial Neural Crest Cells ◽  
Discrete Populations ◽  
Crest Cell

ABSTRACT During craniofacial development, different populations of cartilage- and bone-forming cells develop in precise locations in the head. Most of these cells are derived from pluripotent cranial neural crest cells and differentiate with distinct developmental timing and cellular morphologies. The mechanisms that divide neural crest cells into discrete populations are not fully understood. Here, we use single-cell RNA sequencing to transcriptomically define different populations of cranial neural crest cells. We discovered that the gene family encoding the Alx transcription factors is enriched in the frontonasal population of neural crest cells. Genetic mutant analyses indicate that alx3 functions to regulate the distinct differentiation timing and cellular morphologies among frontonasal neural crest cell subpopulations. This study furthers our understanding of how genes controlling developmental timing shape craniofacial skeletal elements.

scholarly journals Specification of axial identity by Hoxa2 distinguishes between a phenotypic and molecular ground state in mouse cranial neural crest cells

2021 ◽  
Author(s):  
Irina Pushel ◽  
Paul A Trainor ◽  
Robb Krumlauf
Keyword(s):  
Neural Crest ◽  
Ground State ◽  
Molecular Mechanisms ◽  
Neural Crest Cells ◽  
Pharyngeal Arches ◽  
Transcriptional Signature ◽  
Head Formation ◽  
Phenotypic Transformation ◽  
Cranial Neural Crest Cells ◽  
Molecular Ground State

AbstractHox genes play a key role in head formation by specifying the axial identity of neural crest cells (NCCs) migrating into embryonic pharyngeal arches. In the absence of Hoxa2, NCC derivatives of the second pharyngeal arch (PA2) undergo a homeotic transformation and duplicate structures formed by first arch (PA1) NCCs. Current models postulate that PA1 represents a NCC ‘ground state’ and loss of Hoxa2 causes a reversion of PA2 NCCs to the PA1 ‘ground state’. We use bulk and single-cell RNAseq to investigate the molecular mechanisms driving this phenotypic transformation in the mouse. In Hoxa2-/- mutants, PA2 NCCs generally maintain expression of the PA2 transcriptional signature and fail to strongly upregulate a PA1 transcriptional signature. Our analyses identify putative HOXA2 targets and suggest that subsets of NCCs may respond to HOXA2 activity in distinct manners. This separation of phenotypic and molecular states has significant implications for understanding craniofacial 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 Neural crest cells bulldoze through the microenvironment using Aquaporin-1 to stabilize filopodia

2019 ◽  
Author(s):  
Rebecca McLennan ◽  
Mary C. McKinney ◽  
Jessica M. Teddy ◽  
Jason A. Morrison ◽  
Jennifer C. Kasemeier-Kulesa ◽  
...  
Keyword(s):  
Neural Crest ◽  
Protein Function ◽  
Water Channel ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Aquaporin 1 ◽  
Guidance Receptors ◽  
Cranial Neural Crest Cells

ABSTRACTNeural crest migration requires cells to move through an environment filled with dense extracellular matrix and mesoderm to reach targets throughout the vertebrate embryo. Here, we use high-resolution microscopy, computational modeling, and in vitro and in vivo cell invasion assays to investigate the function of Aquaporin-1 (AQP-1) signaling. We find that migrating lead cranial neural crest cells express AQP-1 mRNA and protein, implicating a biological role for water channel protein function during invasion. Differential AQP-1 levels affect neural crest cell speed, direction, and the length and stability of cell filopodia. Further, AQP-1 enhances matrix metalloprotease (MMP) activity and colocalizes with phosphorylated focal adhesion kinases (pFAK). Co-localization of AQP-1 expression with EphB guidance receptors in the same migrating neural crest cells raises novel implications for the concept of guided bulldozing by lead cells during 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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