Analysis of Neural Crest Migration and Differentiation by Cross-species Transplantation

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.

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

Development ◽

10.1242/dev.126.10.2181 ◽

1999 ◽

Vol 126 (10) ◽

pp. 2181-2189 ◽

Cited By ~ 7

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.

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An SEM analysis of neural crest migration in the mouse

Development ◽

10.1242/dev.74.1.97 ◽

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.

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Segmental origin and migration of neural crest cells in the hindbrain region of the chick embryo

Development ◽

10.1242/dev.113.4.1281 ◽

1991 ◽

Vol 113 (4) ◽

pp. 1281-1291 ◽

Cited By ~ 83

Author(s):

A. Lumsden ◽

N. Sprawson ◽

A. Graham

Keyword(s):

Chick Embryo ◽

Neural Crest ◽

Fate Map ◽

Membrane Probe ◽

Vital Dye ◽

Video Fluorescence Microscopy ◽

Dye Analysis ◽

And Migration ◽

Neural Crest Migration ◽

Branchial Region

A vital dye analysis of cranial neural crest migration in the chick embryo has provided a positional fate map of greater resolution than has been possible using labelled graft techniques. Focal injections of the fluorescent membrane probe DiI were made into the cranial neural folds at stages between 3 and 16 somites. Groups of neuroepithelial cells, including the premigratory neural crest, were labelled by the vital dye. Analysis of whole-mount embryos after 1–2 days further development, using conventional and intensified video fluorescence microscopy, revealed the pathways of crest cells migrating from mesencephalic and rhombencephalic levels of the neuraxis into the subjacent branchial region. The patterns of crest emergence and emigration correlate with the segmented disposition of the rhombencephalon. Branchial arches 1, 2 and 3 are filled by crest cells migrating from rhombomeres 2, 4 and 6 respectively, in register with the cranial nerve entry/exit points in these segments. The three streams of ventrally migrating cells are separated by alternating regions, rhombomeres 3 and 5, which release no crest cells. Rostrally, rhombomere 1 and the caudal mesencephalon also contribute crest to the first arch, primarily to its upper (maxillary) component. Both r3 and r5 are associated with enhanced levels of cell death amongst cells of the dorsal midline, suggesting that crest may form at these levels but is then eliminated. Organisation of the branchial region is thus related by the dynamic process of neural crest immigration to the intrinsic mechanisms that segment the neuraxis.

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

Development ◽

10.1242/dev.124.5.949 ◽

1997 ◽

Vol 124 (5) ◽

pp. 949-957 ◽

Cited By ~ 3

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.

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