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.

scholarly journals Effects of Shh and Noggin on neural crest formation demonstrate that BMP is required in the neural tube but not ectoderm

Development ◽  
1998 ◽  
Vol 125 (24) ◽  
pp. 4919-4930 ◽  
Author(s):  
M.A. Selleck ◽  
M.I. Garcia-Castro ◽  
K.B. Artinger ◽  
M. Bronner-Fraser
Keyword(s):  
Neural Crest ◽  
Sonic Hedgehog ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Neural Plate ◽  
Bmp Signaling ◽  
Neural Tube Closure ◽  
Dorsal Neural Tube ◽  
Neural Ectoderm ◽  
Tube Closure

To define the timing of neural crest formation, we challenged the fate of presumptive neural crest cells by grafting notochords, Sonic Hedgehog- (Shh) or Noggin-secreting cells at different stages of neurulation in chick embryos. Notochords or Shh-secreting cells are able to prevent neural crest formation at open neural plate levels, as assayed by DiI-labeling and expression of the transcription factor, Slug, suggesting that neural crest cells are not committed to their fate at this time. In contrast, the BMP signaling antagonist, Noggin, does not repress neural crest formation at the open neural plate stage, but does so if injected into the lumen of the closing neural tube. The period of Noggin sensitivity corresponds to the time when BMPs are expressed in the dorsal neural tube but are down-regulated in the non-neural ectoderm. To confirm the timing of neural crest formation, Shh or Noggin were added to neural folds at defined times in culture. Shh inhibits neural crest production at early stages (0-5 hours in culture), whereas Noggin exerts an effect on neural crest production only later (5-10 hours in culture). Our results suggest three phases of neurulation that relate to neural crest formation: (1) an initial BMP-independent phase that can be prevented by Shh-mediated signals from the notochord; (2) an intermediate BMP-dependent phase around the time of neural tube closure, when BMP-4 is expressed in the dorsal neural tube; and (3) a later pre-migratory phase which is refractory to exogenous Shh and Noggin.

Immunohistochemical localisation of chondroitin sulphate proteoglycans and the effects of chondroitinase ABC in 9- to 11-day rat embryos

Development ◽  
1989 ◽  
Vol 106 (4) ◽  
pp. 787-798
Author(s):  
G. Morriss-Kay ◽  
F. Tuckett
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Chondroitin Sulphate ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Neural Tube Closure ◽  
Chondroitinase Abc ◽  
Rat Embryos ◽  
Crest Cell ◽  
Tube Closure

Studies on cell behaviour in vitro have indicated that the chondroitin sulphate proteoglycan (CSPG) family of molecules can participate in the control of cell proliferation, differentiation and adhesion, but its morphogenetic functions had not been investigated in intact embryos. Chondroitin/chondroitin sulphates have been identified in rat embryos at low levels at the start of neurulation (day 9) and at much higher levels on day 10. In this study we have sought evidence for the morphogenetic functions of CSPGs in rat embryos during the period of neurulation and neural crest cell migration by a combination of two approaches: immunocytochemical localization of CSPG by means of an antibody, CS-56, to the chondroitin sulphate component of CSPG, and exposure of embryos to the enzyme chondroitinase ABC. Staining of the CS-56 epitope was poor at the beginning of cranial neurulation; bright staining was at first confined to the primary mesenchyme under the convex neural folds late on day 9. In day 10 embryos, all mesenchyme cells were stained, but at different levels of intensity, so that primary mesenchyme, neural crest and sclerotomal cells could be distinguished from each other. Basement membranes were also stained, particularly bright staining being present where two epithelial were basally apposed, e.g., neural/surface ectoderms, dorsal aorta/neural tube, prior to migration of a population of cells between them. Staining within the neural epithelium was first confined to the dorsolateral edge region, and associated with the onset of neural crest cell emigration; after neural tube closure, neuroepithelial staining was more general. Neural crest cells were stained during migration, but the reaction was absent in areas associated with migration end-points (trigeminal ganglion anlagen, frontonasal mesenchyme). Embryos exposed to chondroitinase ABC in culture showed no abnormalities until early day 10, when cranial neural crest cell emigration from the neural epithelium was inhibited and neural tube closure was retarded. Sclerotomal cells failed to take their normal pathway between the dorsal aorta and neural tube. Correlation of the results of these two methods suggests: (1) that by decreasing adhesiveness within the neural epithelium at specific stages, CSPG facilitates the emigration of neural crest cells and the migratory movement of neuroblasts, and may also provide increased flexibility during the generation of epithelial curvatures; (2) that by decreasing the adhesiveness of fibronectin-containing extracellular matrices, CSPG facilitates the migration of neural crest and sclerotomal cells. This second function is particularly important when migrating cells take pathways between previously apposed tissues.

scholarly journals Neural crest cell-cell adhesion controlled by sequential and subpopulation-specific expression of novel cadherins

Development ◽  
1995 ◽  
Vol 121 (5) ◽  
pp. 1321-1332 ◽  
Author(s):  
S. Nakagawa ◽  
M. Takeichi
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Specific Interaction ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Neural Tube Closure ◽  
Beta Catenin ◽  
Intercellular Signaling ◽  
Specific Expression ◽  
Cell Cell

We identified two cadherins, c-cad6B and c-cad7, expressed by neural crest cells at their premigratory and migratory stages, respectively, in chicken embryos. cDNA transfection experiments showed that both were homophilic adhesion molecules, endowing cells with specific adhesiveness. During development, c-cad6B appeared in the neural fold, localizing at the future neural crest area. This expression was maintained during neural tube closure, but disappeared after neural crest cells had left the neural tube, suggesting its role in neural fold fusion and/or in the formation and maintenance of the presumptive neural crest domain in the neural plate/tube. Crest cells emerging from the neural tube lost c-cad6B, and a subpopulation of them began to express c-cad7. This subpopulation-specific expression of c-cad7 persisted during their migration. The migrating c-cad7-positive cells clustered together, and eventually populated restricted regions including the dorsal and ventral roots but very little ganglia. The latter was populated with N-cadherin-positive crest cells. Migrating neural crest cells expressed alpha- and beta-catenin at cell-cell contacts, indicating that their cadherins are functioning. These results suggest that the migrating crest cells are grouped into subpopulations expressing different cadherins. The cadherin-mediated specific interaction between crest cells likely plays a role in intercellular signaling between homotypic cells as well as in sorting of heterotypic cells.

scholarly journals Cardiovascular Development and the Colonizing Cardiac Neural Crest Lineage

2007 ◽  
Vol 7 ◽  
pp. 1090-1113 ◽  
Author(s):  
Paige Snider ◽  
Michael Olaopa ◽  
Anthony B. Firulli ◽  
Simon J. Conway
Keyword(s):  
Gene Expression ◽  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Cardiovascular Development ◽  
Cardiac Neural Crest ◽  
Neural Crest Cell Migration ◽  
Crest Cell

Although it is well established that transgenic manipulation of mammalian neural crest-related gene expression and microsurgical removal of premigratory chicken andXenopusembryonic cardiac neural crest progenitors results in a wide spectrum of both structural and functional congenital heart defects, the actual functional mechanism of the cardiac neural crest cells within the heart is poorly understood. Neural crest cell migration and appropriate colonization of the pharyngeal arches and outflow tract septum is thought to be highly dependent on genes that regulate cell-autonomous polarized movement (i.e., gap junctions, cadherins, and noncanonicalWnt1pathway regulators). Once the migratory cardiac neural crest subpopulation finally reaches the heart, they have traditionally been thought to participate in septation of the common outflow tract into separate aortic and pulmonary arteries. However, several studies have suggested these colonizing neural crest cells may also play additional unexpected roles during cardiovascular development and may even contribute to a crest-derived stem cell population. Studies in both mice and chick suggest they can also enter the heart from the venous inflow as well as the usual arterial outflow region, and may contribute to the adult semilunar and atrioventricular valves as well as part of the cardiac conduction system. Furthermore, although they are not usually thought to give rise to the cardiomyocyte lineage, neural crest cells in the zebrafish (Danio rerio) can contribute to the myocardium and may have different functions in a species-dependent context. Intriguingly, both ablation of chick andXenopuspremigratory neural crest cells, and a transgenic deletion of mouse neural crest cell migration or disruption of the normal mammalian neural crest gene expression profiles, disrupts ventral myocardial function and/or cardiomyocyte proliferation. Combined, this suggests that either the cardiac neural crest secrete factor/s that regulate myocardial proliferation, can signal to the epicardium to subsequently secrete a growth factor/s, or may even contribute directly to the heart. Although there are species differences between mouse, chick, and Xenopus during cardiac neural crest cell morphogenesis, recent data suggest mouse and chick are more similar to each other than to the zebrafish neural crest cell lineage. Several groups have used the genetically definedPax3(splotch) mutant mice model to address the role of the cardiac neural crest lineage. Here we review the current literature, the neural crest-related role of thePax3transcription factor, and discuss potential function/s of cardiac neural crest-derived cells during cardiovascular developmental remodeling.

The histogenetic potential of neural plate cells of early-somite-stage mouse embryos

Development ◽  
1986 ◽  
Vol 96 (1) ◽  
pp. 183-193
Author(s):  
W. Y. Chan ◽  
P. P. L. Tam
Keyword(s):  
Neural Crest ◽  
Neural Differentiation ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Neural Plate ◽  
Mouse Embryos ◽  
Renal Capsule ◽  
Somite Stage ◽  
Neural Tissues ◽  
Crest Cell

The mesencephalic neural plate of early-somite-stage mouse embryos differentiated underneath the renal capsule to form mostly neural tissues together with other tissues some of which were probably of neural crest cell origin. The capacity to form non-neural tissues such as skeletal tissues and melanocytes was lost at about the 5-somite stage. The lateral areas of the plate tended to form non-neural tissues more than the medial areas. The cephalic neural plate of presomite head-fold-stage embryos differentiated extensively to form both ectodermal and mesodermal tissues. However, upon completion of neurulation, the mesencephalic neuro-epithelium of forelimb-bud-stage embryos gave rise to neural tissues only. Therefore there is a progressive restriction in the histogenetic capacity of the mesencephalic neural plate during neurulation and this could be attributed to the cellular commitment for neural differentiation and the loss of the neural crest cells.

scholarly journals The vertebrate-specific VENTX/NANOG gene empowers neural crest with ectomesenchyme potential

2020 ◽  
Vol 6 (18) ◽  
pp. eaaz1469 ◽  
Author(s):  
Pierluigi Scerbo ◽  
Anne H. Monsoro-Burq
Keyword(s):  
Neural Crest ◽  
Sensory Neuron ◽  
Neural Crest Cells ◽  
Neural Plate ◽  
Pigment Cells ◽  
Regulatory State ◽  
Neural Plate Border ◽  
Nanog Gene ◽  
Neural Ectoderm

During Cambrian, unipotent progenitors located at the neural (plate) border (NB) of an Olfactoria chordate embryo acquired the competence to form ectomesenchyme, pigment cells and neurons, initiating the rise of the multipotent neural crest cells (NC) specific to vertebrates. Surprisingly, the known vertebrate NB/NC transcriptional circuitry is a constrained feature also found in invertebrates. Therefore, evidence for vertebrate-specific innovations endowing vertebrate NC with multipotency is still missing. Here, we identified VENTX/NANOG and POU5/OCT4 as vertebrate-specific innovations. When VENTX was depleted in vivo and in directly-induced NC, the NC lost its early multipotent state and its skeletogenic potential, but kept sensory neuron and pigment identity, thus reminiscent of invertebrate NB precursors. In vivo, VENTX gain-of-function enabled NB specifiers to reprogram embryonic non-neural ectoderm towards early NC identity. We propose that skeletogenic NC evolved by acquiring VENTX/NANOG activity, promoting a novel multipotent progenitor regulatory state into the pre-existing sensory neuron/pigment NB program.

Zebrafish narrowminded suggests a genetic link between formation of neural crest and primary sensory neurons

Development ◽  
1999 ◽  
Vol 126 (18) ◽  
pp. 3969-3979 ◽  
Author(s):  
K.B. Artinger ◽  
A.B. Chitnis ◽  
M. Mercola ◽  
W. Driever
Keyword(s):  
Neural Crest ◽  
Sensory Neurons ◽  
Cell Formation ◽  
Plate Boundary ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Neural Plate ◽  
Crest Cell

In the developing vertebrate nervous system, both neural crest and sensory neurons form at the boundary between non-neural ectoderm and the neural plate. From an in situ hybridization based expression analysis screen, we have identified a novel zebrafish mutation, narrowminded (nrd), which reduces the number of early neural crest cells and eliminates Rohon-Beard (RB) sensory neurons. Mosaic analysis has shown that the mutation acts cell autonomously suggesting that nrd is involved in either the reception or interpretation of signals at the lateral neural plate boundary. Characterization of the mutant phenotype indicates that nrd is required for a primary wave of neural crest cell formation during which progenitors generate both RB sensory neurons and neural crest cells. Moreover, the early deficit in neural crest cells in nrd homozygotes is compensated later in development. Thus, we propose that a later wave can compensate for the loss of early neural crest cells but, interestingly, not the RB sensory neurons. We discuss the implications of these findings for the possibility that RB sensory neurons and neural crest cells share a common evolutionary origin.

Is there a ventral neural ridge in chick embryos? Implications for the origin of adenohypophyseal and other APUD cells

Development ◽  
1980 ◽  
Vol 57 (1) ◽  
pp. 71-78
Author(s):  
N. B. Levy ◽  
Ann Andrew ◽  
B. B. Rawdon ◽  
Beverley Kramer
Keyword(s):  
Neural Crest ◽  
Endocrine Cells ◽  
Ventral Surface ◽  
Neural Plate ◽  
Chick Embryos ◽  
Serial Sections ◽  
Apud Cells ◽  
Surface Ectoderm ◽  
Neural Ectoderm ◽  
Thickened Surface

Two- to ten-somite chick embryos were studied in order to ascertain whether, as has been proposed, there exists a ‘ventral neural ridge’ which gives rise to the hypophyseal (Rathke's) pouch. Serial sections and stereo-microscopy were used. The neural ridges arch around the rostral end of the embryo onto the ventral surface of the head, but no evidence was found for their extension to form a ‘ventral neural ridge’ reaching the stomodaeum: in fact a considerable expanse of non-thickened surface ectoderm was seen to separate the ventral portions of the neural ridges from the stomodaeum. The thickening of neural ectoderm which does appear on the ventral surface of the head results from apposition and fusion of the opposite neural ridges flanking the neural plate and thus the tip of the anterior neuropore - the classically accepted mode of closure of the neuropore. These findings are in accord with the generally accepted concept of the origin of thehypophyseal pouch rather than with its derivation from a ‘ventral neural ridge’. No sign of neural crest formation was encountered ventrally; this observation excludes the possibility that endocrine cells of the APUD series could originate from neural crest in this region.

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