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

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.

scholarly journals 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

2002 ◽  
Vol 247 (2) ◽  
pp. 251-270 ◽  
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

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

2004 ◽  
Vol 1 (1) ◽  
pp. 57-63 ◽  
Author(s):  
MEYER BAREMBAUM ◽  
MARIANNE BRONNER-FRASER
Keyword(s):  
Neural Crest ◽  
Trigeminal Ganglion ◽  
Neural Tube ◽  
Cell Lineage ◽  
Neural Crest Cells ◽  
Cranial Neural Crest ◽  
Facial Skeleton ◽  
Differentiation Markers ◽  
Branchial Arches ◽  
Cranial Neural Crest Cells

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.

scholarly journals Regulative capacity of the cranial neural tube to form neural crest

Development ◽  
1993 ◽  
Vol 118 (4) ◽  
pp. 1049-1062 ◽  
Author(s):  
T. Scherson ◽  
G. Serbedzija ◽  
S. Fraser ◽  
M. Bronner-Fraser
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Neural Tube Closure ◽  
Dorsal Midline ◽  
Dorsal Neural Tube ◽  
Ventral Neural Tube ◽  
Cranial Neural Crest Cells ◽  
The Relationship ◽  
Regulative Capacity

In avian embryos, cranial neural crest cells emigrate from the dorsal midline of the neural tube shortly after neural tube closure. Previous lineage analyses suggest that the neural crest is not a pre-segregated population of cells within the neural tube; instead, a single progenitor in the dorsal neural tube can contribute to neurons in both the central and the peripheral nervous systems (Bronner-Fraser and Fraser, 1989 Neuron 3, 755–766). To explore the relationship between the ‘premigratory’ neural crest cells and the balance of the cells in the neural tube in the midbrain and hindbrain region, we have challenged the fate of these populations by ablating the neural crest either alone or in combination with the adjoining ventral portions of the neural tube. Focal injections of the vital dye, DiI, into the neural tissue bordering the ablated region demonstrate that cells at the same axial level, in the lateral and ventral neural tube, regulate to reconstitute a population of neural crest cells. These cells emigrate from the neural tube, migrate along normal pathways according to their axial level of origin and appear to give rise to a normal range of derivatives. This regulation following ablation suggests that neural tube cells normally destined to form CNS derivatives can adjust their prospective fates to form PNS and other neural crest derivatives until 4.5-6 hours after the time of normal onset of emigration from the neural tube.

scholarly journals hReg-CNCC reconstructs a regulatory network in human cranial neural crest cells and annotates variants in a developmental context

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Zhanying Feng ◽  
Zhana Duren ◽  
Ziyi Xiong ◽  
Sijia Wang ◽  
Fan Liu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Neural Crest ◽  
Genetic Variants ◽  
Regulatory Network ◽  
Target Genes ◽  
Neural Crest Cells ◽  
Molecular Networks ◽  
Cranial Neural Crest ◽  
Cranial Neural Crest Cells

AbstractCranial Neural Crest Cells (CNCC) originate at the cephalic region from forebrain, midbrain and hindbrain, migrate into the developing craniofacial region, and subsequently differentiate into multiple cell types. The entire specification, delamination, migration, and differentiation process is highly regulated and abnormalities during this craniofacial development cause birth defects. To better understand the molecular networks underlying CNCC, we integrate paired gene expression & chromatin accessibility data and reconstruct the genome-wide human Regulatory network of CNCC (hReg-CNCC). Consensus optimization predicts high-quality regulations and reveals the architecture of upstream, core, and downstream transcription factors that are associated with functions of neural plate border, specification, and migration. hReg-CNCC allows us to annotate genetic variants of human facial GWAS and disease traits with associated cis-regulatory modules, transcription factors, and target genes. For example, we reveal the distal and combinatorial regulation of multiple SNPs to core TF ALX1 and associations to facial distances and cranial rare disease. In addition, hReg-CNCC connects the DNA sequence differences in evolution, such as ultra-conserved elements and human accelerated regions, with gene expression and phenotype. hReg-CNCC provides a valuable resource to interpret genetic variants as early as gastrulation during embryonic development. The network resources are available at https://github.com/AMSSwanglab/hReg-CNCC.

scholarly journals Cadherin-6B proteolysis promotes the neural crest cell epithelial-to-mesenchymal transition through transcriptional regulation

2016 ◽  
Vol 215 (5) ◽  
pp. 735-747 ◽  
Author(s):  
Andrew T. Schiffmacher ◽  
Vivien Xie ◽  
Lisa A. Taneyhill
Keyword(s):  
Neural Crest ◽  
Epithelial To Mesenchymal Transition ◽  
Neural Crest Cell ◽  
Cranial Neural Crest ◽  
Mesenchymal Transition ◽  
Effector Genes ◽  
A Disintegrin And Metalloproteinase ◽  
And Migration ◽  
Cranial Neural Crest Cells

During epithelial-to-mesenchymal transitions (EMTs), cells disassemble cadherin-based junctions to segregate from the epithelia. Chick premigratory cranial neural crest cells reduce Cadherin-6B (Cad6B) levels through several mechanisms, including proteolysis, to permit their EMT and migration. Serial processing of Cad6B by a disintegrin and metalloproteinase (ADAM) proteins and γ-secretase generates intracellular C-terminal fragments (CTF2s) that could acquire additional functions. Here we report that Cad6B CTF2 possesses a novel pro-EMT role by up-regulating EMT effector genes in vivo. After proteolysis, CTF2 remains associated with β-catenin, which stabilizes and redistributes both proteins to the cytosol and nucleus, leading to up-regulation of β-catenin, CyclinD1, Snail2, and Snail2 promoter-based GFP expression in vivo. A CTF2 β-catenin–binding mutant, however, fails to alter gene expression, indicating that CTF2 modulates β-catenin–responsive EMT effector genes. Notably, CTF2 association with the endogenous Snail2 promoter in the neural crest is β-catenin dependent. Collectively, our data reveal how Cad6B proteolysis orchestrates multiple pro-EMT regulatory inputs, including CTF2-mediated up-regulation of the Cad6B repressor Snail2, to ensure proper cranial neural crest EMT.

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