scholarly journals Endothelin-B receptor is expressed by neural crest cells in the avian embryo.

1996 ◽  
Vol 93 (18) ◽  
pp. 9645-9650 ◽  
Author(s):  
V. Nataf ◽  
L. Lecoin ◽  
A. Eichmann ◽  
N. M. Le Douarin
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Avian Embryo ◽  
Endothelin B Receptor ◽  
Endothelin B

Pax3 is required for cardiac neural crest migration in the mouse: evidence from the splotch (Sp2H) mutant

Development ◽  
1997 ◽  
Vol 124 (2) ◽  
pp. 505-514 ◽  
Author(s):  
S.J. Conway ◽  
D.J. Henderson ◽  
A.J. Copp
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Outflow Tract ◽  
Avian Embryo ◽  
Cardiac Neural Crest ◽  
Branchial Arches ◽  
Aortic Arches ◽  
Cardiac Outflow

Neural crest cells originating in the occipital region of the avian embryo are known to play a vital role in formation of the septum of the cardiac outflow tract and to contribute cells to the aortic arches, thymus, thyroid and parathyroids. This ‘cardiac’ neural crest sub-population is assumed to exist in mammals, but without direct evidence. In this paper we demonstrate, using RT-PCR and in situ hybridisation, that Pax3 expression can serve as a marker of cardiac neural crest cells in the mouse embryo. Cells of this lineage were traced from the occipital neural tube, via branchial arches 3, 4 and 6, into the aortic sac and aorto-pulmonary outflow tract. Confirmation that these Pax3-positive cells are indeed cardiac neural crest is provided by experiments in which hearts were deprived of a source of colonising neural crest, by organ culture in vitro, with consequent lack of up-regulation of Pax3. Occipital neural crest cell outgrowths in vitro were also shown to express Pax3. Mutation of Pax3, as occurs in the splotch (Sp2H) mouse, results in development of conotruncal heart defects including persistent truncus arteriosus. Homozygotes also exhibit defects of the aortic arches, thymus, thyroid and parathyroids. Pax3-positive neural crest cells were found to emigrate from the occipital neural tube of Sp2H/Sp2H embryos in a relatively normal fashion, but there was a marked deficiency or absence of neural crest cells traversing branchial arches 3, 4 and 6, and entering the cardiac outflow tract. This decreased expression of Pax3 in Sp2H/Sp2H embryos was not due to down-regulation of Pax3 in neural crest cells, as use of independent neural crest markers, Hoxa-3, CrabpI, Prx1, Prx2 and c-met also revealed a deficiency of migrating cardiac neural crest cells in homozygous embryos. This work demonstrates the essential role of the cardiac neural crest in formation of the heart and great vessels in the mouse and, furthermore, shows that Pax3 function is required for the cardiac neural crest to complete its migration to the developing heart.

The developmental fate of the cephalic mesoderm in quail-chick chimeras

Development ◽  
1992 ◽  
Vol 114 (1) ◽  
pp. 1-15 ◽  
Author(s):  
G.F. Couly ◽  
P.M. Coltey ◽  
N.M. Le Douarin
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Paraxial Mesoderm ◽  
Avian Embryo ◽  
Facial Skeleton ◽  
Developmental Fate ◽  
Prechordal Mesoderm ◽  
The Face ◽  
Neural Crest Origin ◽  
Neurula Stage

The developmental fate of the cephalic paraxial and prechordal mesoderm at the late neurula stage (3-somite) in the avian embryo has been investigated by using the isotopic, isochronic substitution technique between quail and chick embryos. The territories involved in the operation were especially tiny and the size of the transplants was of about 150 by 50 to 60 microns. At that stage, the neural crest cells have not yet started migrating and the fate of mesodermal cells exclusively was under scrutiny. The prechordal mesoderm was found to give rise to the following ocular muscles: musculus rectus ventralis and medialis and musculus oblicus ventralis. The paraxial mesoderm was separated in two longitudinal bands: one median, lying upon the cephalic vesicles (median paraxial mesoderm—MPM); one lateral, lying upon the foregut (lateral paraxial mesoderm—LPM). The former yields the three other ocular muscles, contributes to mesencephalic meninges and has essentially skeletogenic potencies. It contributes to the corpus sphenoid bone, the orbitosphenoid bone and the otic capsules; the rest of the facial skeleton is of neural crest origin. At 3-somite stage, MPM is represented by a few cells only. The LPM is more abundant at that stage and has essentially myogenic potencies with also some contribution to connective tissue. However, most of the connective cells associated with the facial and hypobranchial muscles are of neural crest origin. The more important result of this work was to show that the cephalic mesoderm does not form dermis. This function is taken over by neural crest cells, which form both the skeleton and dermis of the face. If one draws a parallel between the so-called “somitomeres” of the head and the trunk somites, it appears that skeletogenic potencies are reduced in the former, which in contrast have kept their myogenic capacities, whilst the formation of skeleton and dermis has been essentially taken over by the neural crest in the course of evolution of the vertebrate head.

Spatial and temporal distribution of vinculin and talin in migrating avian neural crest cells and their derivatives

Development ◽  
1990 ◽  
Vol 108 (3) ◽  
pp. 421-433
Author(s):  
J.L. Duband ◽  
J.P. Thiery
Keyword(s):  
Neural Crest ◽  
Expression Patterns ◽  
Temporal Distribution ◽  
Neural Crest Cells ◽  
Cell Types ◽  
Avian Embryo ◽  
Sensory Ganglia ◽  
Adhesive Properties ◽  
Final Destination ◽  
Derivatives Of

Neural crest cells express different adhesion modes at each phase of their development starting with their separation from the neural tube, followed by migration along definite pathways throughout the embryo, and finally to settlement and differentiation in elected embryonic regions. In order to determine possible changes in the cytoskeleton organization and function during these processes, we have studied the in situ distribution of two major cytoskeleton-associated elements involved in the membrane anchorage of actin microfilaments, i.e. vinculin and talin, during the ontogeny of the neural crest and its derivatives in the avian embryo. Prior to emigration, neural crest cells exhibited both vinculin and talin at levels similar to the neighbouring neural epithelial cells, and this expression apparently did not change as cells became endowed with migratory properties. However, vinculin became selectively enhanced in neural crest cells as they further migrated towards their final destination. This increase in vinculin amount was particularly striking in vagal and truncal neural crest cells entering cellular environments, such as the sclerotome and the gut mesenchyme. Talin was also expressed by neural crest cells but, in contrast to vinculin, staining was not conspicuous compared to neighbouring mesenchymal cells. High levels of vinculin persisted throughout embryogenesis in almost all neural derivatives of the neural crest, including the autonomous and sensory ganglia and Schwann cells along the peripheral nerves. In contrast, the non-neural derivatives of the neural crest rapidly lost their prominent vinculin staining after migration. The pattern of talin in the progeny of the neural crest was complex and varied with the cell types: for example, some cranial sensory ganglia expressed high amounts of the molecule whereas autonomic ganglia were nearly devoid of it. Our results suggest that (i) vinculin and talin may follow independent regulatory patterns within the same cell population, (ii) the level of expression of vinculin and talin in neural crest cells may be consistent with the rapid, constant modulations of their adhesive properties, and (iii) the expression patterns of the two molecules may also be correlated with the genesis of the peripheral nervous system.

scholarly journals Expression of endothelin 3 by mesenchymal cells of embryonic mouse caecum

Gut ◽  
1999 ◽  
Vol 44 (2) ◽  
pp. 246-252 ◽  
Author(s):  
M A Leibl ◽  
T Ota ◽  
M N Woodward ◽  
S E Kenny ◽  
D A Lloyd ◽  
...  
Keyword(s):  
Neural Crest ◽  
Protein Tyrosine Kinase ◽  
In Situ Hybridisation ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Mesenchymal Cells ◽  
Paracrine Factor ◽  
Embryonic Mouse ◽  
Endothelin B ◽  
Endothelin 3

BackgroundMutations in endothelin 3 (EDN3) and endothelin B receptor (EDNRB) genes cause terminal colonic aganglionosis in mice, and mutations in these genes have also been linked to the terminal aganglionosis seen in human Hirschsprung’s disease. However, details of EDN3 expression during embryogenesis are lacking, and consequently the cellular mechanism by which EDN3 regulates innervation of the terminal gut is unclear.AimsTo localise the expression of EDN3 and EDNRB in the embryonic mouse gut.MethodsExpression of EDN3 and EDNRB mRNA was analysed by reverse transcription polymerase chain reaction and in situ hybridisation.ResultsHigh levels of EDN3 mRNA expression were restricted to mesenchymal cells of the caecum before and after the arrival of neural crest cells. In contrast, EDNRB expression along the gut displayed a time dependent pattern similar to those of the protein tyrosine kinase ret and the neural crest cell marker PGP9.5.ConclusionsMesenchymal cells of the caecum express high levels of EDN3 mRNA during embryogenesis and hence the production of EDN3 at the caecum is likely to act on neural crest cells as a paracrine factor necessary for subsequent innervation of the terminal gut.

scholarly journals Migrating neural crest cells in the trunk of the avian embryo are multipotent

Development ◽  
1991 ◽  
Vol 112 (4) ◽  
pp. 913-920 ◽  
Author(s):  
S.E. Fraser ◽  
M. Bronner-Fraser
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Sympathetic Neurons ◽  
Morphological Characteristics ◽  
Neural Crest Cells ◽  
Cell Types ◽  
Sympathetic Ganglia ◽  
Avian Embryo ◽  
Developmental Potential ◽  
Trunk Neural Crest

Trunk neural crest cells migrate extensively and give rise to diverse cell types, including cells of the sensory and autonomic nervous systems. Previously, we demonstrated that many premigratory trunk neural crest cells give rise to descendants with distinct phenotypes in multiple neural crest derivatives. The results are consistent with the idea that neural crest cells are multipotent prior to their emigration from the neural tube and become restricted in phenotype after leaving the neural tube either during their migration or at their sites of localization. Here, we test the developmental potential of migrating trunk neural crest cells by microinjecting a vital dye, lysinated rhodamine dextran (LRD), into individual cells as they migrate through the somite. By two days after injection, the LRD-labelled clones contained from 2 to 67 cells, which were distributed unilaterally in all embryos. Most clones were confined to a single segment, though a few contributed to sympathetic ganglia over two segments. A majority of the clones gave rise to cells in multiple neural crest derivatives. Individual migrating neural crest cells gave rise to both sensory and sympathetic neurons (neurofilament-positive), as well as cells with the morphological characteristics of Schwann cells, and other non-neuronal cells (both neurofilament-negative). Even those clones contributing to only one neural crest derivative often contained both neurofilament-positive and neurofilament-negative cells. Our data demonstrate that migrating trunk neural crest cells can be multipotent, giving rise to cells in multiple neural crest derivatives, and contributing to both neuronal and non-neuronal elements within a given derivative.(ABSTRACT TRUNCATED AT 250 WORDS)

Avian neural crest cells can migrate in the dorsolateral path only if they are specified as melanocytes

Development ◽  
1995 ◽  
Vol 121 (3) ◽  
pp. 915-924 ◽  
Author(s):  
C.A. Erickson ◽  
T.L. Goins
Keyword(s):  
Neural Crest ◽  
Normal Development ◽  
Neural Crest Cells ◽  
Pigment Cells ◽  
Environmental Cues ◽  
Avian Embryo ◽  
Thoracic Level ◽  
Branchial Arches ◽  
Trunk Neural Crest ◽  
Migratory Pathway

Neural crest cells are conventionally believed to migrate arbitrarily into various pathways and to differentiate according to the environmental cues that they encounter. We present data consistent with the notion that melanocytes are directed, by virtue of their phenotype, into the dorsolateral path, whereas other neural crest derivatives are excluded. In the avian embryo, trunk neural crest cells that migrate ventrally differentiate largely into neurons and glial cells of the peripheral nervous system. Neural crest cells that migrate into the dorsolateral path become melanocytes, the pigment cells of the skin. Neural crest cells destined for the dorsolateral path are delayed in their migration until at least 24 hours after migration commences ventrally. Previous studies have suggested that invasion into the dorsolateral path is dependent upon a change in the migratory environment. A complementary possibility is that as neural crest cells differentiate into melanocytes they acquire the ability to take this pathway. When quail neural crest cells that have been grown in culture for 12 hours are labeled with Fluoro-gold and then grafted into the early migratory pathway at the thoracic level, they migrate only ventrally and are coincident with the host neural crest. When fully differentiated melanocytes (96 hours old) are back-grafted under identical conditions, however, they enter the dorsolateral path and invade the ectoderm at least one day prior to the host neural crest. Likewise, neural crest cells that have been cultured for at least 20 hours and are enriched in melanoblasts immediately migrate in the dorsolateral path, in addition to the ventral path, when back-grafted into the thoracic level. A population of neural crest cells depleted of melanoblasts--crest cells derived from the branchial arches--are not able to invade the dorsolateral path, suggesting that only pigment cells or their precursors are able to take this migratory route. These results suggest that as neural crest cells differentiate into melanocytes they can exploit the dorsolateral path immediately. Even when 12-hour crest cells are grafted into stage 19–21 embryos at an axial level where host crest are invading the dorsolateral path, these young neural crest cells do not migrate dorsolaterally. Conversely, melanoblasts or melanocytes grafted under the same circumstances are found in the ectoderm. These latter results suggest that during normal development neural crest cells must be specified, if not already beginning to differentiate, as melanocytes in order to take this path.(ABSTRACT TRUNCATED AT 400 WORDS)

The migration of neural crest cells to the wall of the digestive tract in avian embryo

Development ◽  
1973 ◽  
Vol 30 (1) ◽  
pp. 31-48
Author(s):  
Nicole M. Le Douarin ◽  
Marie-Aimée Teillet
Keyword(s):  
Neural Crest ◽  
Ganglion Cells ◽  
Neural Crest Cells ◽  
Avian Embryo ◽  
Somite Stage ◽  
Neuroblast Migration ◽  
Enteric Ganglia ◽  
Neural Axis ◽  
Hind Gut

Isotopic and isochronic grafts of quail neural primordium in chick embryos have been made. Due to the particular structure of their nuclei, quail cells can be distinguished from chick cells and so be used as natural markers to study the migration of neural crest cells. We have been able to demonstrate by this technique that the parasympathetic enteric ganglion cells arise from two different levels of the embryonic neural axis which correspond to the vagal and lumbo-sacral parasympathetic centres. The main source of the enteric neuroblasts is located at the level of the somites 1–7. It gives rise to ganglion cells which migrate in the whole gut including the large intestine and rectum. The other region from which enteric neuroblasts originate is situated behind the level of the 28th somite and gives rise only to some post-umbilical gut ganglion cells. In this region of the intestine the ganglia are made up of a mixture of cells arising from the vagal and the lumbo-sacral levels of the neural axis. The part of the neural primordium between the 8th and the 28th somite does not participate in the formation of the enteric ganglia. The chronology of the enteric neuroblast migration has been studied. Most cells of vagal origin leave the neural crest before the 13-somite stage but the migration lasts sometimes until after the 16-somite stage. Those cells which have to reach the hind-gut level accomplish a long-term migration which can be evaluated at 6 days or more. The presumptive neuroblasts of lumbo-sacral origin are not found in the hind-gut before the 7th day of incubation. In our experiments we have never observed the migration of any quail cells into the endoderm of the chick host embryo. Therefore we consider that enterochromaffin cells of the digestive epithelium are not derived from the levels of the neural crest concerned in these experiments (i.e. rhombencephalic and medullary Anlagen).

Spatiotemporal changes in HNK-1/L2 glycoconjugates on avian embryo somite and neural crest cells

1990 ◽  
Vol 139 (1) ◽  
pp. 100-120 ◽  
Author(s):  
D.F. Newgreen ◽  
M.E. Powell ◽  
B. Moser
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Avian Embryo ◽  
Spatiotemporal Changes

scholarly journals Rhombomere of origin determines autonomous versus environmentally regulated expression of Hoxa-3 in the avian embryo

Development ◽  
1996 ◽  
Vol 122 (3) ◽  
pp. 895-904 ◽  
Author(s):  
J.R. Saldivar ◽  
C.E. Krull ◽  
R. Krumlauf ◽  
L. Ariza-McNaughton ◽  
M. Bronner-Fraser
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Branchial Arch ◽  
Normal Embryo ◽  
Avian Embryo ◽  
Boundary Formation ◽  
Environmental Signals ◽  
Cell Autonomy ◽  
Short Time

We have investigated the pattern and regulation of Hoxa3 expression in the hindbrain and associated neural crest cells in the chick embryo, using whole mount in situ hybridization in conjunction with DiI labeling of neural crest cells and microsurgical manipulations. Hoxa3 is expressed in the neural plate and later in the neural tube with a rostral border of expression corresponding to the boundary between rhombomeres (r) 4 and 5. Initial expression is diffuse and becomes sharp after boundary formation. Hoxa3 exhibits uniform expression within r5 after formation of rhombomeric borders. Cell marking experiments reveal that neural crest cells migrating caudally, but not rostrally, from r5 and caudally from r6 express Hoxa3 in normal embryo. Results from transposition experiments demonstrate that expression of Hoxa3 in r5 neural crest cells is not strictly cell-autonomous. When r5 is transposed with r4 by rostrocaudal rotation of the rhomobomeres, Hoxa3 is expressed in cells migrating lateral to transposed r5 and for a short time, in condensing ganglia, but not by neural crest within the second branchial arch. Since DiI-labeled cells from transposed r5 are present in the second arch, Hoxa3-expressing neural crest cells from r5 appear to down-regulate their Hoxa3 expression in their new environment. In contrast, when r6 is transposed to the position of r4 after boundary formation, Hoxa3 is maintained in both migrating neural crest cells and those positioned within the second branchial arch and associated ganglia. These results suggest that Hoxa3 expression is cell-autonomous in r6 and its associated neural crest. Our results suggest that neural crest cells expressing the same Hox gene are not eqivalent; they respond differently to environmental signals and exhibit distinct degrees of cell autonomy depending upon their rhombomere of origin.

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.

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