The origin of intrinsic ganglia of trunk viscera from vagal neural crest in the chick embryo

1954 ◽  
Vol 101 (2) ◽  
pp. 515-541 ◽  
Author(s):  
Chester L. Yntema ◽  
Warner S. Hammond
Keyword(s):  
Chick Embryo ◽  
Neural Crest ◽  
Intrinsic Ganglia

Non-malignant migration of B16 mouse melanoma cells in the neural crest and invasive growth in the eye cup of the chick embryo

2007 ◽  
Vol 17 (1) ◽  
pp. 17-30 ◽  
Author(s):  
Matthias Oppitz ◽  
Christian Busch ◽  
Gernot Schriek ◽  
Marco Metzger ◽  
Lothar Just ◽  
...  
Keyword(s):  
Chick Embryo ◽  
Neural Crest ◽  
Melanoma Cells ◽  
Invasive Growth ◽  
Mouse Melanoma ◽  
B16 Mouse Melanoma

Overexpression of Snail family members highlights their ability to promote chick neural crest formation

Development ◽  
2002 ◽  
Vol 129 (7) ◽  
pp. 1583-1593 ◽  
Author(s):  
Marta G. del Barrio ◽  
M. Angela Nieto
Keyword(s):  
Chick Embryo ◽  
Neural Crest ◽  
Neural Tube ◽  
Family Members ◽  
Ectopic Expression ◽  
Endogenous Gene ◽  
The Family ◽  
Snail Family ◽  
Migratory Cells ◽  
Snail Gene

The Snail gene family of transcription factors plays crucial roles in different morphogenetic processes during the development of vertebrate and invertebrate embryos. In previous studies of function interference for one of the family members, Slug, we showed its involvement and neural crest formation in the chick embryo. Now we have carried out a series of gain-of-function experiments in which we show that Slug overexpression in the neural tube of the chick embryo induces an increase in neural crest production. The analysis of electroporated embryos shows that Slug can induce the expression of rhoB and an increase in the number of HNK-1-positive migratory cells, indicating that it lies upstream of them in the genetic cascade of neural crest development. The increase in neural crest production after Slug overexpression was confined to the cranial region, indicating that the mechanisms of crest induction somehow differ between head and trunk. The expression of the two vertebrate family members, Slug and Snail, is peculiar with respect to the neural crest. Slug is not expressed in the premigratory crest in the mouse, whereas it is expressed in this cell population in the chick and the opposite is true for Snail(Sefton, M., Sánchez, S. and Nieto M. A. (1998) Development125, 3111-3121). This raises the question of whether they can be functionally equivalent. To test this hypothesis both intra- and interspecies, we have performed a series of ectopic expression experiments by electroporating chick and mouse Snail in the chick embryo hindbrain. We observe that both genes elicit the same responses in the neural tube. Our results indicate that they can be functionally equivalent, although the embryos show a higher response to the endogenous gene, chick Slug.

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

Development ◽  
1991 ◽  
Vol 113 (4) ◽  
pp. 1281-1291 ◽  
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.

The differing effects of occipital and trunk somites on neural development in the chick embryo

Development ◽  
1987 ◽  
Vol 100 (3) ◽  
pp. 525-533 ◽  
Author(s):  
T.M. Lim ◽  
E.R. Lunn ◽  
R.J. Keynes ◽  
C.D. Stern
Keyword(s):  
Chick Embryo ◽  
Neural Crest ◽  
Neural Tube ◽  
Neural Development ◽  
Osmium Tetroxide ◽  
Local Property ◽  
Sensory Cells ◽  
Base Of The Skull ◽  
Atlas And Axis ◽  
Zinc Iodide

In all higher vertebrate embryos the sensory ganglia of the trunk develop adjacent to the neural tube, in the cranial halves of the somite-derived sclerotomes. It has been known for many years that ganglia do not develop in the most cranial (occipital) sclerotomes, caudal to the first somite. Here we have investigated whether this is due to craniocaudal variation in the neural tube or crest, or to an unusual property of the sclerotomes at occipital levels. Using the monoclonal antibody HNK-1 as a marker for neural crest cells in the chick embryo, we find that the crest does enter the cranial halves of the occipital sclerotomes. Furthermore, staining with zinc iodide/osmium tetroxide shows that some of these crest-derived cells sprout axons within these sclerotomes. By stage 23, however, no dorsal root ganglia are present within the five occipital sclerotomes, as assessed both by haematoxylin/eosin and zinc iodide/osmium tetroxide staining. Moreover, despite this loss of sensory cells, motor axons grow out in these segments, many of them later fasciculating to form the hypoglossal nerve. The sclerotomes remain visible until stages 27/28, when they dissociate to form the base of the skull and the atlas and axis vertebrae. After grafting occipital neural tube from quail donor embryos in place of trunk neural tube in host chick embryos, quail-derived ganglia do develop in the trunk sclerotomes. This shows that the failure of occipital ganglion development is not the result of some fixed local property of the neural crest or neural tube at occipital levels. We therefore suggest that in the chick embryo the cranial halves of the five occipital sclerotomes lack factors essential for normal sensory ganglion development, and that these factors are correspondingly present in all the more caudal sclerotomes.

Interactions between rhombomeres modulate Krox-20 and follistatin expression in the chick embryo hindbrain

Development ◽  
1996 ◽  
Vol 122 (2) ◽  
pp. 473-480 ◽  
Author(s):  
A. Graham ◽  
A. Lumsden
Keyword(s):  
Chick Embryo ◽  
Neural Crest ◽  
Cell Lineage ◽  
Signalling Molecule ◽  
Neighbour Interaction

The rhombomeres of the embryonic hindbrain display compartment properties, including cell lineage restriction, genetic definition and modular anatomical phenotype. Consistent with the idea that rhombomeres are autonomous developmental units, previous studies have shown that certain aspects of rhombomere phenotype are determined early, at the time of rhombomere formation. By contrast, the apoptotic depletion of neural crest from rhombomeres 3 and 5 is due to an interaction with their neighbouring rhombomeres, involving the signalling molecule Bmp4. In this paper, we have examined whether inter-rhombomere interactions control further aspects of rhombomere phenotype. We find that the expression of Krox-20 and the repression of follistatin in r3 is dependent upon neighbour interaction, whereas these genes are expressed autonomously in r5. We further demonstrate that modulation of Krox-20 and follistatin expression is not dependent on Bmp4, indicating the existence of multiple pathways of interaction between adjacent rhombomeres. We also show that, although some phenotypic aspects of r3 are controlled by neighbour interactions, the axial identity of the segment is intrinsically determined.

Ectodermal patterning in the avian embryo: epidermis versus neural plate

Development ◽  
1999 ◽  
Vol 126 (1) ◽  
pp. 63-73 ◽  
Author(s):  
E. Pera ◽  
S. Stein ◽  
M. Kessel
Keyword(s):  
Chick Embryo ◽  
Neural Crest ◽  
Plate Boundary ◽  
Homeobox Gene ◽  
Primitive Streak ◽  
Neural Plate ◽  
Avian Embryo ◽  
Neural Fate ◽  
Early Stages ◽  
Two Factors

Ectodermal patterning of the chick embryo begins in the uterus and continues during gastrulation, when cells with a neural fate become restricted to the neural plate around the primitive streak, and cells fated to become the epidermis to the periphery. The prospective epidermis at early stages is characterized by the expression of the homeobox gene DLX5, which remains an epidermal marker during gastrulation and neurulation. Later, some DLX5-expressing cells become internalized into the ventral forebrain and the neural crest at the hindbrain level. We studied the mechanism of ectodermal patterning by transplantation of Hensen's nodes and prechordal plates. The DLX5 marker indicates that not only a neural plate, but also a surrounding epidermis is induced in such operations. Similar effects can be obtained with neural plate grafts. These experiments demonstrate that the induction of a DLX5-positive epidermis is triggered by the midline, and the effect is transferred via the neural plate to the periphery. By repeated extirpations of the endoderm we suppressed the formation of an endoderm/mesoderm layer under the epiblast. This led to the generation of epidermis, and to the inhibition of neuroepithelium in the naked ectoderm. This suggests a signal necessary for neural, but inhibitory for epidermal development, normally coming from the lower layers. Finally, we demonstrate that BMP4, as well as BMP2, is capable of inducing epidermal fate by distorting the epidermis-neural plate boundary. This, however, does not happen independently within the neural plate or outside the normal DLX5 domain. In the area opaca, the co-transplantation of a BMP4 bead with a node graft leads to the induction of DLX5, thus indicating the cooperation of two factors. We conclude that ectodermal patterning is achieved by signalling both from the midline and from the periphery, within the upper but also from the lower layers.

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