scholarly journals In Vivo Quantitative Imaging Provides Insights into Trunk Neural Crest Migration

Cell Reports ◽  
2019 ◽  
Vol 26 (6) ◽  
pp. 1489-1500.e3 ◽  
Author(s):  
Yuwei Li ◽  
Felipe M. Vieceli ◽  
Walter G. Gonzalez ◽  
Ang Li ◽  
Weiyi Tang ◽  
...  
Keyword(s):  
Neural Crest ◽  
Quantitative Imaging ◽  
Trunk Neural Crest ◽  
Neural Crest Migration

scholarly journals Neuromesodermal Progenitor Origin of Trunk Neural Crest in vivo

2021 ◽  
Author(s):  
Martyna Lukoseviciute ◽  
Sarah Mayes ◽  
Tatjana Sauka-Spengler
Keyword(s):  
Neural Crest ◽  
Trunk Neural Crest

An SEM analysis of neural crest migration in the mouse

Development ◽  
1983 ◽  
Vol 74 (1) ◽  
pp. 97-118
Author(s):  
C. A. Erickson ◽  
J. A. Weston
Keyword(s):  
Neural Crest ◽  
Basal Lamina ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Sem Analysis ◽  
Basement Membranes ◽  
Dorsal Neural Tube ◽  
Trunk Neural Crest ◽  
Unique Cell ◽  
Neural Crest Migration

The cellular morphology and migratory pathways of the trunk neural crest are described in normal mouse embryos, and in embryos homozygous for Patch in which neural crest derivatives develop abnormally. Trunk neural crest cells initially appear in 8½-day embryos as a unique cell population on the dorsal neural tube surface and are relatively rounded. Once they begin to migrate the cells flatten and orient somewhat tangentially to the neural tube, and advance ventrad between the somites and neural tube. At the onset of migration neural crest cells extend lamellipodia onto the surface of the tube while detaching their trailing processes from the lumenal surface. The basal lamina on the dorsal neural tube is discontinuous when cell migration begins in this region. As development proceeds, the basal lamina gradually becomes continuous from a lateral to dorsal direction and neural crest emigration is progressively confined to the narrowing region of discontinuous basal lamina. Cell separation from the neural tube ceases concomitant with completion of a continuous basement membrane. Preliminary observations of the mutant embryos reveal that abnormal extracellular spaces appear and patterns of crest migration are subsequently altered. We conclude that the extracellular matrix, extracellular spaces and basement membranes may delimit crest migration in the mouse.

scholarly journals Gap Junction–mediated Cell–Cell Communication Modulates Mouse Neural Crest Migration

1998 ◽  
Vol 143 (6) ◽  
pp. 1725-1734 ◽  
Author(s):  
G.Y. Huang ◽  
E.S. Cooper ◽  
K. Waldo ◽  
M.L. Kirby ◽  
N.B. Gilula ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Neural Crest ◽  
Gap Junction ◽  
Heart Defects ◽  
Neural Crest Cells ◽  
Dominant Negative ◽  
Cardiac Neural Crest ◽  
Gap Junction Communication ◽  
Neural Crest Migration

Previous studies showed that conotruncal heart malformations can arise with the increase or decrease in α1 connexin function in neural crest cells. To elucidate the possible basis for the quantitative requirement for α1 connexin gap junctions in cardiac development, a neural crest outgrowth culture system was used to examine migration of neural crest cells derived from CMV43 transgenic embryos overexpressing α1 connexins, and from α1 connexin knockout (KO) mice and FC transgenic mice expressing a dominant-negative α1 connexin fusion protein. These studies showed that the migration rate of cardiac neural crest was increased in the CMV43 embryos, but decreased in the FC transgenic and α1 connexin KO embryos. Migration changes occurred in step with connexin gene or transgene dosage in the homozygous vs. hemizygous α1 connexin KO and CMV43 embryos, respectively. Dye coupling analysis in neural crest cells in the outgrowth cultures and also in the living embryos showed an elevation of gap junction communication in the CMV43 transgenic mice, while a reduction was observed in the FC transgenic and α1 connexin KO mice. Further analysis using oleamide to downregulate gap junction communication in nontransgenic outgrowth cultures showed that this independent method of reducing gap junction communication in cardiac crest cells also resulted in a reduction in the rate of crest migration. To determine the possible relevance of these findings to neural crest migration in vivo, a lacZ transgene was used to visualize the distribution of cardiac neural crest cells in the outflow tract. These studies showed more lacZ-positive cells in the outflow septum in the CMV43 transgenic mice, while a reduction was observed in the α1 connexin KO mice. Surprisingly, this was accompanied by cell proliferation changes, not in the cardiac neural crest cells, but in the myocardium— an elevation in the CMV43 mice vs. a reduction in the α1 connexin KO mice. The latter observation suggests that cardiac neural crest cells may have a role in modulating growth and development of non–neural crest– derived tissues. Overall, these findings suggest that gap junction communication mediated by α1 connexins plays an important role in cardiac neural crest migration. Furthermore, they indicate that cardiac neural crest perturbation is the likely underlying cause for heart defects in mice with the gain or loss of α1 connexin function.

scholarly journals Protein Tyrosine Phosphatase 4A3 (PTP4A3) Is Required for Xenopus laevis Cranial Neural Crest Migration In Vivo

PLoS ONE ◽  
2013 ◽  
Vol 8 (12) ◽  
pp. e84717 ◽  
Author(s):  
Selma Maacha ◽  
Nathalie Planque ◽  
Cécile Laurent ◽  
Caterina Pegoraro ◽  
Océane Anezo ◽  
...  
Keyword(s):  
Xenopus Laevis ◽  
Neural Crest ◽  
Protein Tyrosine Phosphatase ◽  
Tyrosine Phosphatase ◽  
Cranial Neural Crest ◽  
Protein Tyrosine ◽  
Neural Crest Migration

scholarly journals Chick cranial neural crest cells migrate by progressively refining the polarity of their protrusions

2017 ◽  
Author(s):  
Miriam A. Genuth ◽  
Christopher D.C. Allen ◽  
Takashi Mikawa ◽  
Orion D. Weiner
Keyword(s):  
Neural Crest ◽  
Quantitative Imaging ◽  
Cell Movement ◽  
Neural Crest Cells ◽  
Branchial Arch ◽  
Cranial Neural Crest ◽  
Directed Movement ◽  
Morphological Polarity ◽  
Cranial Neural Crest Cells

SummaryIn vivo quantitative imaging reveals that chick cranial neural crest cells throughout the migratory stream are morphologically polarized and migrate by progressively refining the polarity of their protrusions.AbstractTo move directionally, cells can bias the generation of protrusions or select among randomly generated protrusions. Here we use 3D two-photon imaging of chick branchial arch 2 directed neural crest cells to probe how these mechanisms contribute to directed movement, whether a subset or the majority of cells polarize during movement, and how the different classes of protrusions relate to one another. We find that cells throughout the stream are morphologically polarized along the direction of overall stream movement and that there is a progressive sharpening of the morphological polarity program. Neural crest cells have weak spatial biases in filopodia generation and lifetime. Local bursts of filopodial generation precede the generation of larger protrusions. These larger protrusions are more spatially biased than the filopodia, and the subset of protrusions that power motility are the most polarized of all. Orientation rather than position is the best correlate of the protrusions that are selected for cell movement. This progressive polarity refinement strategy may enable neural crest cells to efficiently explore their environment and migrate accurately in the face of noisy guidance cues.

scholarly journals Soluble and cell-bound forms of steel factor activity play distinct roles in melanocyte precursor dispersal and survival on the lateral neural crest migration pathway

Development ◽  
1995 ◽  
Vol 121 (3) ◽  
pp. 731-742 ◽  
Author(s):  
B. Wehrle-Haller ◽  
J.A. Weston
Keyword(s):  
Neural Crest ◽  
Neural Crest Cell ◽  
Soluble Form ◽  
Steel Factor ◽  
Migration Pathway ◽  
Staging Area ◽  
Trunk Neural Crest ◽  
Membrane Bound ◽  
Neural Crest Migration

Trunk neural crest cells segregate from the neuroepithelium and enter a ‘migration staging area’ lateral to the embryonic neural tube. After some crest cells in the migration staging area have begun to migrate on a medial pathway, a subpopulation of crest-derived cells remaining in the migration staging area expresses mRNAs for the receptor tyrosine kinase, c-kit, and tyrosinase-related protein-2, both of which are characteristic of melanocyte precursors. These putative melanocyte precursors are subsequently observed on the lateral crest migration pathway between the dermatome and overlying epithelium, and then dispersed in nascent dermal mesenchyme. Melanocyte precursors transiently require the c-kit ligand, Steel factor for survival. Although Steel factor mRNA is transiently expressed in the dorsal dermatome before the onset of trunk neural crest cell dispersal on the lateral pathway, it is no longer produced by dermatomal cells when melanocyte precursors have dispersed in the dermal mesenchyme. To assess the role of Steel factor in migration of melanocyte precursors on the lateral pathway, we analyzed melanocyte precursor dispersal and fate on the lateral pathway of two different Sl mutants, Sl, a null allele, and Sld, which lacks cell surface-associated Steel factor but produces a soluble form. No melanocyte precursors were detected in the dermatome of embryos homozygous for the Sl allele or in W mutants that lack functional c-kit. In contrast, in embryos homozygous for the Sld allele, melanocyte precursors appeared on the lateral pathway, but subsequently disappear from the dermis. These results suggest that soluble Steel factor is required for melanocyte precursor dispersal on the lateral pathway, or for their initial survival in the migration staging area. In contrast, membrane-bound Steel factor appears to promote melanocyte precursor survival in the dermis.

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