Avian neural crest-derived neurogenic precursors undergo apoptosis on the lateral migration pathway

Development ◽  
1998 ◽  
Vol 125 (21) ◽  
pp. 4205-4213 ◽  
Author(s):  
Y. Wakamatsu ◽  
M. Mochii ◽  
K.S. Vogel ◽  
J.A. Weston
Keyword(s):  
Neural Crest ◽  
Environmental Factor ◽  
Neuronal Cells ◽  
Neural Crest Cells ◽  
Lateral Migration ◽  
Avian Embryos ◽  
Migration Pathway ◽  
Proof Reading ◽  
Vertebrate Embryos ◽  
And Function

Neural crest cells of vertebrate embryos disperse on distinct pathways and produce different derivatives in specific embryonic locations. In the trunk of avian embryos, crest-derived cells that initially migrate on the lateral pathway, between epidermal ectoderm and somite, produce melanocytes but no neuronal derivatives. Although we found that melanocyte precursors are specified before they disperse on the lateral pathway, we also observed that a few crest-derived neuronal cells are briefly present on the same pathway. Here, we show that neuronal cells are removed by an episode of apoptosis. These observations suggest that localized environmental factor(s) affect the distribution of fate-restricted crest derivatives and function as a ‘proof-reading mechanism’ to remove ‘ectopic’ crest-derived cells.

Neural crest cells and skeletogenesis in vertebrate embryos

1981 ◽  
Vol 13 (4) ◽  
pp. 631-642 ◽  
Author(s):  
Peter Thorogood
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Vertebrate Embryos

Control of N-cadherin-mediated intercellular adhesion in migrating neural crest cells in vitro

1995 ◽  
Vol 108 (12) ◽  
pp. 3839-3853 ◽  
Author(s):  
F. Monier-Gavelle ◽  
J.L. Duband
Keyword(s):  
Neural Crest ◽  
Tyrosine Kinases ◽  
Brefeldin A ◽  
Neural Crest Cells ◽  
Cell Aggregation ◽  
Phosphatase Inhibitors ◽  
Intercellular Contacts ◽  
And Function ◽  
Cell Cell

Dispersion of neural crest cells and their ultimate regroupment into peripheral ganglia are associated with precisely coordinated regulations both in time and space of the expression and function of cell adhesion receptors. In particular, the disappearance of N-cadherin from the cell surface at the onset of migration and its reexpression during cell aggregation suggest that, during migration, N-cadherin expression is repressed in neural crest cells. In the present study, we have analyzed in vitro the mechanism of control of N-cadherin expression and function in migrating neural crest cells. Although these cells moved as a dense population, each individual did not establish extensive and permanent intercellular contacts with its neighbors. However, cells synthesized and expressed mature N-cadherin molecules at levels comparable to those found in cells that exhibit stable intercellular contacts, but in contrast to them, the bulk of N-cadherin molecules was not connected with the cytoskeleton. We next determined which intracellular events are responsible for the instability of the N-cadherin junctions in neural crest cells using various chemical agents known to affect signal transduction processes. Agents that block a broad spectrum of serine-threonine kinases (6-dimethylaminopurine, H7 and staurosporine) or that affect selectively protein kinases C (bisindolylmaleimide and sphingosine), inhibitors of protein tyrosine kinases (erbstatin, herbimycin A, and tyrphostins), and inhibitors of phosphatases (vanadate) all restored tight cell-cell associations among neural crest cells, accompanied by a slight increase in the overall cellular content of N-cadherin and its accumulation to the regions of intercellular contacts. The effect of the kinase and phosphatase blockers was inhibitable by agents known to affect protein synthesis (cycloheximide) and exportation (brefeldin A), indicating that the restored cell-cell contacts were mediated chiefly by an intracellular pool of N-cadherin molecules recruited to the membrane. Finally, N-cadherin molecules were constitutively phosphorylated in migrating neural crest cells, but their level and state of phosphorylation were apparently not modified in the presence of kinase and phosphatase inhibitors. These observations therefore suggest that N-cadherin-mediated cell-cell interactions are not stable in neural crest cells migrating in vitro, and that they are under the control of a complex cascade of intracellular signals involving kinases and phosphatases and probably elicited by surface receptors.

Migration of Enteric Neural Crest Cells in Relation to Growth of the Gut in Avian Embryos

1996 ◽  
Vol 157 (2) ◽  
pp. 105-115 ◽  
Author(s):  
D.F. Newgreen ◽  
B. Southwell ◽  
L. Hartley ◽  
I.J. Allan
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Avian Embryos

scholarly journals Early specification of sensory neuron fate revealed by expression and function of neurogenins in the chick embryo

Development ◽  
1999 ◽  
Vol 126 (8) ◽  
pp. 1715-1728 ◽  
Author(s):  
S.E. Perez ◽  
S. Rebelo ◽  
D.J. Anderson
Keyword(s):  
Neural Crest ◽  
Sensory Neuron ◽  
Ectopic Expression ◽  
Neural Crest Cells ◽  
Sensory Ganglia ◽  
Helix Loop Helix ◽  
Autonomic Neurons ◽  
And Function ◽  
Bhlh Transcription Factors

The generation of sensory and autonomic neurons from the neural crest requires the functions of two classes of basic helix-loop-helix (bHLH) transcription factors, the Neurogenins (NGNs) and MASH-1, respectively (Fode, C., Gradwohl, G., Morin, X., Dierich, A., LeMeur, M., Goridis, C. and Guillemot, F. (1998) Neuron 20, 483–494; Guillemot, F., Lo, L.-C., Johnson, J. E., Auerbach, A., Anderson, D. J. and Joyner, A. L. (1993) Cell 75, 463–476; Ma, Q., Chen, Z. F., Barrantes, I. B., de la Pompa, J. L. and Anderson, D. J. (1998 Neuron 20, 469–482). We have cloned two chick NGNs and found that they are expressed in a subset of neural crest cells early in their migration. Ectopic expression of the NGNs in vivo biases migrating neural crest cells to localize in the sensory ganglia, and induces the expression of sensory neuron-appropriate markers in non-sensory crest derivatives. Surprisingly, the NGNs can also induce the expression of multiple pan-neuronal and sensory-specific markers in the dermomyotome, a mesodermal derivative. Taken together, these data suggest that a subset of neural crest cells may already be specified for a sensory neuron fate early in migration, as a consequence of NGN expression.

Regulated expression of neurofibromin in migrating neural crest cells of avian embryos

1995 ◽  
Vol 27 (4) ◽  
pp. 535-552 ◽  
Author(s):  
Kate M. Stocker ◽  
Lawrence Baizer ◽  
Tiffani Coston ◽  
Larry Sherman ◽  
Gary Ciment
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Avian Embryos ◽  
Regulated Expression

Analysis of the origins and early fates of neural crest cells in caudal regions of avian embryos

1985 ◽  
Vol 110 (2) ◽  
pp. 467-479 ◽  
Author(s):  
Gary C. Schoenwolf ◽  
Nancy B. Chandler ◽  
Jodi L. Smith
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Avian Embryos

scholarly journals A transition from SoxB1 to SoxE transcription factors is essential for progression from pluripotent blastula cells to neural crest cells

2018 ◽  
Author(s):  
Elsy Buitrago-Delgado ◽  
Elizabeth N. Schock ◽  
Kara Nordin ◽  
Carole LaBonne
Keyword(s):  
Transcription Factors ◽  
Neural Crest ◽  
Es Cells ◽  
Neural Crest Cells ◽  
Stem Cell Population ◽  
Striking Difference ◽  
Neuronal Progenitor ◽  
Hand Off ◽  
Pluripotency Gene ◽  
Vertebrate Embryos

AbstractThe neural crest is a stem cell population unique to vertebrate embryos that gives rise to derivatives from multiple embryonic germ layers. The molecular underpinnings of potency that govern neural crest potential are highly conserved with that of pluripotent blastula stem cells, suggesting that neural crest cells may have evolved through retention of aspects of the pluripotency gene regulatory network (GRN). A striking difference in the regulatory factors utilized in pluripotent blastula cells and neural crest cells is the deployment of different subfamilies of Sox transcription factors; SoxB1 factors play central roles in the pluripotency of naïve blastula and ES cells, whereas neural crest cells require SoxE function. Here we explore the shared and distinct activities of these factors to shed light on the role that this molecular hand-off of Sox factor activity plays in the genesis of neural crest and the lineages derived from it. Our findings provide evidence that SoxB1 and SoxE factors have both overlapping and distinct activities in regulating pluripotency and lineage restriction in the embryo. We hypothesize that SoxE factors may transiently replace SoxB1 factors to control pluripotency in neural crest cells, and then poise these cells to contribute to glial, chondrogenic and melanocyte lineages at stages when SoxB1 factors promote neuronal progenitor formation.

scholarly journals Mitf-family transcription factor function is required within cranial neural crest cells to promote choroid fissure closure

2019 ◽  
Author(s):  
Katie L. Sinagoga ◽  
Alessandra M. Larimer-Picciani ◽  
Stephanie M. George ◽  
Samantha A. Spencer ◽  
James A. Lister ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Neural Crest ◽  
Neural Crest Cells ◽  
Cranial Neural Crest ◽  
Cellular Mechanisms ◽  
Optic Cup ◽  
Summary Statement ◽  
Cranial Neural Crest Cells ◽  
And Function ◽  
Choroid Fissure

AbstractA critical step in eye development is closure of the choroid fissure (CF), a transient structure in the ventral optic cup through which vasculature enters the eye and ganglion cell axons exit. While many factors have been identified that function during CF closure, the molecular and cellular mechanisms mediating this process remain poorly understood. Failure of CF closure results in colobomas. Recently, MITF was shown to be mutated in a subset of human coloboma patients, but how MITF functions during CF closure is unknown. To address this question, zebrafish with mutations in mitfa and tfec, two members of the Mitf-family of transcription factors, were analyzed and their functions during CF closure determined. mitfa;tfec mutants possess severe colobomas and our data demonstrate that Mitf activity is required within cranial neural crest cells (cNCCs) to facilitate CF closure. In the absence of Mitf function, cNCC migration and localization in the optic cup are perturbed. These data shed light on the cellular mechanisms underlying colobomas in patients with MITF mutations and identify a novel role for Mitf function in cNCCs during CF closure.Summary StatementMitf-family transcription factors act within cranial neural crest cells to promote choroid fissure closure. Without Mitf-family function, cNCC localization and function in the CF is disrupted, thus contributing to colobomas.

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