Melanoblast-tissue interactions and the development of pigment pattern in Xenopus larvae

Development ◽  
1976 ◽  
Vol 35 (3) ◽  
pp. 463-484
Author(s):  
Gillian J. MacMillan
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Population Pressure ◽  
Primary Host ◽  
Pigment Pattern ◽  
Embryonic Tissues ◽  
Tissue Interactions ◽  
Species Specific ◽  
Almost All ◽  
Neural Crest Migration

The melanophores of larval Xenopus laevis are disparately distributed on the hypomere in that the upper region (UHT) is densely pigmented, the median region (MHT) is moderately pigmented, and the lower region (LHT) is unpigmented. The roles of the melanoblasts and their tissue environment in determining the melanophore pattern was investigated by heterotopic transplantation of hypomeric tissues, culture of neural crest explants in vesicles derived from hypomeric tissues and radioactive marking of neural crest cells. Somite-situated grafts of UHT, MHT and LHT were found to possess melanophore densities similar to those exhibited by such hypomeric tissues when in their normal situation. The number and distribution of trunk melanophores in ‘crestless’ second host larvae bearing grafts of UHT, MHT and LHT transferred from the somites of primary host embryos indicated that (a) many melanoblasts entered all transplants during neural crest migration in the primary host: subsequently, a small number of melanoblasts were lost from transplants of UHT, a greater number from transplants of MHT and almost all from transplants of LHT; (b) almost all melanoblasts migrated out from transplants of MHT and LHT and entered the tissues of the ‘crestless’ host, whereas a considerable number of melanoblasts remained in the transplant when it was formed from UHT. Grafts of UHT placed mid-ventrally in the hypomere failed to exhibit melanophores. Vesicles of (a) UHT + MHT and (b) LHT containing neural crest tissue possessed similar numbers of melanophores. Vesicles of LHT differed from those of UHT + MHT in that melanophores were densely aggregated in the implanted neural tissues. Following radioactive marking of neural crest cells labelled nuclei were found on the dorsal ridges of the somites, the surfaces of the neural tube and notochord and in the mesoderm of the upper hypomere and the fin, but were absent from the lateral surfaces of the somites. These results showed that the melanophore pattern in larval Xenopus depended upon melanoblast-tissue interactions, which influenced the migration, rather than the differentiation, proliferation or destruction, of melanoblasts and suggested that tissue selection by migrating melanoblasts enabled these cells to distribute themselves in embryonic tissues in accordance with a hierarchy of melanoblast-tissue affinities. Melanoblast-tissue affinities appeared to be related to the adhesiveness of mesodermal cells: melanoblast extensibility appeared to facilitate exploration of the surrounding tissues. The formation of pigment pattern in larval Xenopus appeared to depend upon the interaction between the melanoblast population pressure and melanoblast-tissue affinities. The present results and those of other workers on amphibian pigmentation were used toconstruct a model capable of accounting for species-specific differences in larval amphibian pigment patterns, in terms of interactions between species-specific differences in melanoblast-tissue affinities and melanoblast population pressure.

An experimental study on neural crest migration in Barbus conchonius (Cyprinidae, Teleostei), with special reference to the origin of the enteroendocrine cells

Development ◽  
1981 ◽  
Vol 62 (1) ◽  
pp. 309-323
Author(s):  
C. H. J. Lamers ◽  
J. W. H. M. Rombout ◽  
L. P. M. Timmermans
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Ganglion Cells ◽  
Neural Crest Cells ◽  
Enteroendocrine Cells ◽  
Pigment Cells ◽  
Transplantation Technique ◽  
Spinal Ganglion Cells ◽  
Neural Crest Origin ◽  
Neural Crest Migration

A neural crest transplantation technique is described for fish. As in other classes ofvertebrates, two pathways of neural crest migration can be distinguished: a lateroventral pathway between somites and ectoderm, and a medioventral pathway between somites and neural tube/notochord. In this paper evidence is presented for a neural crest origin of spinal ganglion cells and pigment cells, and indication for such an origin is obtained for sympathetic and enteric ganglion cells and for cells that are probably homologues to adrenomedullary and paraganglion cells in the future kidney area. The destiny of neural crest cells near the developing lateral-line sense organs is discussed. When grafted into the yolk, neural crest cells or neural tube cells appear to differentiate into ‘periblast cells’; this suggests a highly activating influence of the yolk. Many neural crest cells are found around the urinary ducts and, when grafted below the notochord, even within the urinary duct epithelium. These neural crest cells do not invade the gut epithelium, even when grafted adjacent to the developing gut. Consequently enteroendocrine cells in fish are not likely to have a trunkor rhombencephalic neural crest origin. Another possible origin of these cells will be proposed.

scholarly journals Origins of the avian neural crest: the role of neural plate-epidermal interactions

Development ◽  
1995 ◽  
Vol 121 (2) ◽  
pp. 525-538 ◽  
Author(s):  
M.A. Selleck ◽  
M. Bronner-Fraser
Keyword(s):  
Neural Crest ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Neural Plate ◽  
Neural Tube Closure ◽  
Whole Embryo Culture ◽  
Early Stages ◽  
Tissue Interactions ◽  
Neural Ectoderm

We have investigated the lineage and tissue interactions that result in avian neural crest cell formation from the ectoderm. Presumptive neural plate was grafted adjacent to non-neural ectoderm in whole embryo culture to examine the role of tissue interactions in ontogeny of the neural crest. Our results show that juxtaposition of non-neural ectoderm and presumptive neural plate induces the formation of neural crest cells. Quail/chick recombinations demonstrate that both the prospective neural plate and the prospective epidermis can contribute to the neural crest. When similar neural plate/epidermal confrontations are performed in tissue culture to look at the formation of neural crest derivatives, juxtaposition of epidermis with either early (stages 4–5) or later (stages 6–10) neural plate results in the generation of both melanocytes and sympathoadrenal cells. Interestingly, neural plates isolated from early stages form no neural crest cells, whereas those isolated later give rise to melanocytes but not crest-derived sympathoadrenal cells. Single cell lineage analysis was performed to determine the time at which the neural crest lineage diverges from the epidermal lineage and to elucidate the timing of neural plate/epidermis interactions during normal development. Our results from stage 8 to 10+ embryos show that the neural plate/neural crest lineage segregates from the epidermis around the time of neural tube closure, suggesting that neural induction is still underway at open neural plate stages.

Evidence for collapsin-1 functioning in the control of neural crest migration in both trunk and hindbrain regions

Development ◽  
1999 ◽  
Vol 126 (10) ◽  
pp. 2181-2189 ◽  
Author(s):  
B.J. Eickholt ◽  
S.L. Mackenzie ◽  
A. Graham ◽  
F.S. Walsh ◽  
P. Doherty
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Axon Growth ◽  
Neural Crest Cells ◽  
Neural Crest Cell Migration ◽  
Neural Crest Migration ◽  
Migration Pathways ◽  
Crest Cell

Collapsin-1 belongs to the Semaphorin family of molecules, several members of which have been implicated in the co-ordination of axon growth and guidance. Collapsin-1 can function as a selective chemorepellent for sensory neurons, however, its early expression within the somites and the cranial neural tube (Shepherd, I., Luo, Y., Raper, J. A. and Chang, S. (1996) Dev. Biol. 173, 185–199) suggest that it might contribute to the control of additional developmental processes in the chick. We now report a detailed study on the expression of collapsin-1 as well as on the distribution of collapsin-1-binding sites in regions where neural crest cell migration occurs. collapsin-1 expression is detected in regions bordering neural crest migration pathways in both the trunk and hindbrain regions and a receptor for collapsin-1, neuropilin-1, is expressed by migrating crest cells derived from both regions. When added to crest cells in vitro, a collapsin-1-Fc chimeric protein induces morphological changes similar to those seen in neuronal growth cones. In order to test the function of collapsin-1 on the migration of neural crest cells, an in vitro assay was used in which collapsin-1-Fc was immobilised in alternating stripes consisting of collapsin-Fc/fibronectin versus fibronectin alone. Explanted neural crest cells derived from both trunk and hindbrain regions avoided the collapsin-Fc-containing substratum. These results suggest that collapsin-1 signalling can contribute to the patterning of neural crest cell migration in the developing chick.

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.

Mechanisms of Neural Crest Migration

2018 ◽  
Vol 52 (1) ◽  
pp. 43-63 ◽  
Author(s):  
András Szabó ◽  
Roberto Mayor
Keyword(s):  
Neural Crest ◽  
Cell Population ◽  
Epithelial To Mesenchymal Transition ◽  
Neural Crest Cells ◽  
Cell Types ◽  
Embryonic Cell ◽  
Mesenchymal Transition ◽  
Chain Migration ◽  
Mass Migration ◽  
Neural Crest Migration

Neural crest cells are a transient embryonic cell population that migrate collectively to various locations throughout the embryo to contribute a number of cell types to several organs. After induction, the neural crest delaminates and undergoes an epithelial-to-mesenchymal transition before migrating through intricate yet characteristic paths. The neural crest exhibits a variety of migratory behaviors ranging from sheet-like mass migration in the cephalic regions to chain migration in the trunk. During their journey, neural crest cells rely on a range of signals both from their environment and within the migrating population for navigating through the embryo as a collective. Here we review these interactions and mechanisms, including chemotactic cues of neural crest cells’ migration.

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 The hypoxia factor Hif-1α controls neural crest chemotaxis and epithelial to mesenchymal transition

2013 ◽  
Vol 201 (5) ◽  
pp. 759-776 ◽  
Author(s):  
Elias H. Barriga ◽  
Patrick H. Maxwell ◽  
Ariel E. Reyes ◽  
Roberto Mayor
Keyword(s):  
Neural Crest ◽  
Cancer Metastasis ◽  
Epithelial To Mesenchymal Transition ◽  
Neural Crest Cells ◽  
Embryonic Cell ◽  
Zebrafish Embryos ◽  
Mesenchymal Transition ◽  
Metastasis Inhibition ◽  
Neural Crest Migration ◽  
Transcription Factor 1

One of the most important mechanisms that promotes metastasis is the stabilization of Hif-1 (hypoxia-inducible transcription factor 1). We decided to test whether Hif-1α also was required for early embryonic development. We focused our attention on the development of the neural crest, a highly migratory embryonic cell population whose behavior has been likened to cancer metastasis. Inhibition of Hif-1α by antisense morpholinos in Xenopus laevis or zebrafish embryos led to complete inhibition of neural crest migration. We show that Hif-1α controls the expression of Twist, which in turn represses E-cadherin during epithelial to mesenchymal transition (EMT) of neural crest cells. Thus, Hif-1α allows cells to initiate migration by promoting the release of cell–cell adhesions. Additionally, Hif-1α controls chemotaxis toward the chemokine SDF-1 by regulating expression of its receptor Cxcr4. Our results point to Hif-1α as a novel and key regulator that integrates EMT and chemotaxis during migration of neural crest cells.

Growth of Neural Crest Cells In Vitro Is Enhanced By Extracts From Silky Fowl Embryonic Tissues

1994 ◽  
Vol 7 (4) ◽  
pp. 210-216 ◽  
Author(s):  
LAURE LECOIN ◽  
PASCALE MERCIER ◽  
NICOLE M. LE DOUARIN
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Embryonic Tissues
Sign in / Sign up

Export Citation Format

Share Document