scholarly journals Segmental migration of trunk neural crest: time-lapse analysis reveals a role for PNA-binding molecules

Development ◽  
1995 ◽  
Vol 121 (11) ◽  
pp. 3733-3743 ◽  
Author(s):  
C.E. Krull ◽  
A. Collazo ◽  
S.E. Fraser ◽  
M. Bronner-Fraser
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Time Lapse ◽  
Light Level ◽  
Explant Culture ◽  
Peanut Agglutinin ◽  
Trunk Neural Crest ◽  
Neural Crest Migration ◽  
Molecular Bases ◽  
First Time

Trunk neural crest cells migrate through the somites in a striking segmental fashion, entering the rostral but not caudal sclerotome, via cues intrinsic to the somites. Attempts to define the molecular bases of these cues have been hampered by the lack of an accessible assay system. To examine trunk neural crest migration over time and to perturb candidate guiding molecules, we have developed a novel explant preparation. Here, we demonstrate that trunk regions of the chicken embryo, placed in explant culture, continue to develop apparently normally for 2 days. Neural crest cells, recognized by prelabeling with DiI or by poststaining with the HNK-1 antibody, migrate in the somites of the explants in their typical segmental pattern. Furthermore, this paradigm allows us to follow trunk neural crest migration in situ for the first time using low-light-level videomicroscopy. The trajectories of individual neural crest cells were often complex, with cells migrating in an episodic mode encompassing forward, backward and lateral movements. Frequently, neural crest cells migrated in close-knit groups of 2–4 cells, moving at mean rates of migration of 10–14 microns/hour. Treatment of the explants with the lectin peanut agglutinin (PNA) both slowed the rate and altered the pattern of neural crest migration. Neural crest cells entered both the rostral and caudal halves of the sclerotome with mean rates of migration ranging from 6 to 13 microns/hour. These results suggest that peanut agglutinin-binding molecules are required for the segmental patterning of trunk neural crest migration. Because this approach permits neural crest migration to be both observed and perturbed, it offers the promise of more direct assays of the factors that influence neural crest development.

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.

Glycoconjugates mark a transient barrier to neural crest migration in the chicken embryo

Development ◽  
1994 ◽  
Vol 120 (1) ◽  
pp. 103-114 ◽  
Author(s):  
R.A. Oakley ◽  
C.J. Lasky ◽  
C.A. Erickson ◽  
K.W. Tosney
Keyword(s):  
Neural Crest ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Experimental Manipulation ◽  
Binding Activity ◽  
Cell Entry ◽  
Avian Embryo ◽  
Peanut Agglutinin ◽  
Neural Crest Migration ◽  
Crest Cell

We report that two molecular markers correlate with a transient inhibition of neural crest cell entry into the dorsolateral path between the ectoderm and the somite in the avian embryo. During the period when neural crest cells are excluded from the dorsolateral path, both peanut agglutinin lectin (PNA)-binding activity and chondroitin-6-sulfate (C6S) immunoreactivity are expressed within this path. Both markers decline as neural crest cells enter. Moreover, both markers are absent after an experimental manipulation that accelerates neural crest entry into this path. Specifically, dermamyotome deletions abolish expression of both markers and allow neural crest cells to enter the dorsolateral path precociously. After partial deletions, dermatome remnants remain. These remnants retain PNA and C6S labeling and impede migration locally. Local glycoconjugate expression thus correlates directly with avoidance responses. Since both PNA-binding activity and C6S expression also typify inhibitory somitic tissues, molecules indicated by these markers (or co-regulated molecules) are likely to inhibit both neural crest and axon advance.

Migration of cardiac neural crest cells in Splotch embryos

Development ◽  
2000 ◽  
Vol 127 (9) ◽  
pp. 1869-1878 ◽  
Author(s):  
J.A. Epstein ◽  
J. Li ◽  
D. Lang ◽  
F. Chen ◽  
C.B. Brown ◽  
...  
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Explant Culture ◽  
Outflow Tract ◽  
Fine Tuning ◽  
Fate Map ◽  
Cardiac Neural Crest ◽  
Neural Crest Migration ◽  
Derivatives Of

Pax3 encodes a transcription factor expressed during mid-gestation in the region of the dorsal neural tube that gives rise to migrating neural crest populations. In the absence of Pax3, both humans and mice develop with neural crest defects. Homozygous Splotch embryos that lack Pax3 die by embryonic day 13.5 with cardiac defects that resemble those induced by neural crest ablation in chick models. This has led to the hypothesis that Pax3 is required for cardiac neural crest migration. However, cardiac derivatives of Pax3-expressing precursor cells have not been previously defined, and Pax3-expressing cells within the heart have not been well demonstrated. Hence, the precise role of Pax3 during cardiac development remains unclear. Here, we use a Cre-lox method to fate map Pax3-expressing neural crest precursors to the cardiac outflow tract. We show that although Pax3 itself is extinguished prior to neural crest populating the heart, derivatives of these precursors contribute to the aorticopulmonary septum. We further show that neural crest cells are found in the outflow tract of Splotch embryos, albeit in reduced numbers. This indicates that contrary to prior reports, Pax3 is not required for cardiac neural crest migration. Using a neural tube explant culture assay, we demonstrate that neural crest cells from Splotch embryos show normal rates of proliferation but altered migratory characteristics. These studies suggest that Pax3 is required for fine tuning the migratory behavior of the cardiac neural crest cells while it is not essential for neural crest migration.

scholarly journals Molecular and Cellular Features of Murine Craniofacial and Trunk Neural Crest Cells as Stem Cell-Like Cells

PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e84072 ◽  
Author(s):  
Kunie Hagiwara ◽  
Takeshi Obayashi ◽  
Nobuyuki Sakayori ◽  
Emiko Yamanishi ◽  
Ryuhei Hayashi ◽  
...  
Keyword(s):  
Stem Cell ◽  
Neural Crest ◽  
Neural Crest Cells ◽  
Trunk Neural Crest

scholarly journals Characterization of late emerging trunk neural crest cells in the turtle Trachemys scripta

2010 ◽  
Vol 344 (1) ◽  
pp. 531
Author(s):  
Judith A. Cebra-Thomas ◽  
James Robinson ◽  
Melinda Yin ◽  
James McCarthy ◽  
Sonal Shah ◽  
...  
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Trachemys Scripta ◽  
Trunk Neural Crest

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 Matrigel supports neural, melanocytic and chondrogenic differentiation of trunk neural crest cells

2013 ◽  
Vol 57 (11-12) ◽  
pp. 885-890 ◽  
Author(s):  
Ana B. Ramos-Hryb ◽  
Meline C. Da-Costa ◽  
Andréa G. Trentin ◽  
Giordano W. Calloni
Keyword(s):  
Neural Crest ◽  
Chondrogenic Differentiation ◽  
Neural Crest Cells ◽  
Trunk Neural Crest

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.

Taste buds develop autonomously from endoderm without induction by cephalic neural crest or paraxial mesoderm

Development ◽  
1997 ◽  
Vol 124 (5) ◽  
pp. 949-957 ◽  
Author(s):  
L.A. Barlow ◽  
R.G. Northcutt
Keyword(s):  
Epithelial Cells ◽  
Neural Crest ◽  
Explant Culture ◽  
Nerve Fibers ◽  
Taste Buds ◽  
Paraxial Mesoderm ◽  
Culture Techniques ◽  
Well Differentiated ◽  
Neural Crest Migration

Although it had long been believed that embryonic taste buds in vertebrates were induced to differentiate by ingrowing nerve fibers, we and others have recently shown that embryonic taste buds can develop normally in the complete absence of innervation. This leads to the question of which tissues, if any, induce the formation of taste buds in oropharyngeal endoderm. We proposed that taste buds, like many specialized epithelial cells, might arise via an inductive interaction between the endodermal epithelial cells that line the oropharynx and the adjacent mesenchyme that is derived from both cephalic neural crest and paraxial mesoderm. Using complementary grafting and explant culture techniques, however, we have now found that well-differentiated taste buds will develop in tissue completely devoid of neural crest and paraxial mesoderm derivatives. When the presumptive oropharyngeal region was removed from salamander embryos prior to the onset of cephalic neural crest migration, taste buds developed in grafts and explants coincident with their appearance in intact control embryos. Similarly, explants from neurulae in which movement of paraxial mesoderm had not yet begun also developed taste buds after 9–12 days in vitro. We conclude that neither cranial neural crest nor paraxial mesoderm is responsible for the induction of embryonic taste buds. Surprisingly, the ability to develop taste buds late in embryonic development seems to be an intrinsic feature of the oropharyngeal endoderm that is determined by the completion of gastrulation.

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.

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