A morphological and experimental study of the mesencephalic neural crest cells in the mouse embryo using wheat germ agglutinin-gold conjugate as the cell marker

Development ◽  
1988 ◽  
Vol 102 (2) ◽  
pp. 427-442 ◽  
Author(s):  
W.Y. Chan ◽  
P.P. Tam
Keyword(s):  
Neural Crest ◽  
Trigeminal Ganglion ◽  
Mouse Embryo ◽  
Neural Crest Cells ◽  
Cell Interaction ◽  
Paraxial Mesoderm ◽  
Pharyngeal Arch ◽  
Cell Marker ◽  
Gold Conjugate ◽  
Specific Labelling

The distribution of the mesencephalic neural crest cells in the mouse embryo was studied by mapping the colonization pattern of WGA-gold labelled cells following specific labelling of the neuroectoderm and grafting of presumptive neural crest cells to orthotopic and heterotopic sites. The result showed that (1) there were concomitant changes in the morphology of the neural crest epithelium during the formation of neural crest cells, in the 4- to 7-somite-stage embryos, (2) the neural crest cells were initially confined to the lateral subectodermal region of the cranial mesenchyme and there was minimal mixing with the paraxial mesoderm underneath the neural plate, (3) labelled cells from the presumptive crest region colonized the lateral cranio-facial mesenchyme, the developing trigeminal ganglion and the pharyngeal arch, (4) the formation of neural crest cells was facilitated by the focal disruption of the basal lamina and the cell-cell interaction specific to the neural crest site and (5) the trigeminal ganglion was colonized not only by neural crest cells but also by cells from the ectodermal placode.

Cranial paraxial mesoderm and neural crest cells of the mouse embryo: co-distribution in the craniofacial mesenchyme but distinct segregation in branchial arches

Development ◽  
1995 ◽  
Vol 121 (8) ◽  
pp. 2569-2582 ◽  
Author(s):  
P.A. Trainor ◽  
P.P. Tam
Keyword(s):  
Neural Crest ◽  
Mouse Embryo ◽  
Neural Crest Cells ◽  
Paraxial Mesoderm ◽  
Cell Populations ◽  
Cell Labelling ◽  
Mouse Development ◽  
Branchial Arches ◽  
Early Mouse ◽  
Derivatives Of

The spatial distribution of the cranial paraxial mesoderm and the neural crest cells during craniofacial morphogenesis of the mouse embryo was studied by micromanipulative cell grafting and cell labelling. Results of this study show that the paraxial mesoderm and neural crest cells arising at the same segmental position share common destinations. Mesodermal cells from somitomeres I, III, IV and VI were distributed to the same craniofacial tissues as neural crest cells of the forebrain, the caudal midbrain, and the rostral, middle and caudal hindbrains found respectively next to these mesodermal segments. This finding suggests that a basic meristic pattern is established globally in the neural plate ectoderm and paraxial mesoderm during early mouse development. Cells from these two sources mixed extensively in the peri-ocular, facial, periotic and cervical mesenchyme. However, within the branchial arches a distinct segregation of these two cell populations was discovered. Neural crest cells colonised the periphery of the branchial arches and enveloped the somitomere-derived core tissues on the rostral, lateral and caudal sides of the arch. Such segregation of cell populations in the first three branchial arches is apparent at least until the 10.5-day hindlimb bud stage and could be important for the patterning of the skeletal and myogenic derivatives of the arches.

scholarly journals Avian neural crest cell attachment to laminin: involvement of divalent cation dependent and independent integrins

Development ◽  
1991 ◽  
Vol 113 (4) ◽  
pp. 1069-1084 ◽  
Author(s):  
T. Lallier ◽  
M. Bronner-Fraser
Keyword(s):  
Neural Crest ◽  
Cell Attachment ◽  
Divalent Cations ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Cell Interaction ◽  
Cell Binding ◽  
Cell Adherence ◽  
Beta 1 Integrin ◽  
Crest Cell

The mechanisms of neural crest cell interaction with laminin were explored using a quantitative cell attachment assay. With increasing substratum concentrations, an increasing percentage of neural crest cells adhere to laminin. Cell adhesion at all substratum concentrations was inhibited by the CSAT antibody, which recognizes the chick beta 1 subunit of integrin, suggesting that beta 1-integrins mediate neural crest cell interactions with laminin. The HNK-1 antibody, which recognizes a carbohydrate epitope, inhibited neural crest cell attachment to laminin at low coating concentrations (greater than 1 microgram ml-1; Low-LM), but not at high coating concentration of laminin (10 micrograms ml-1; High-LM). Attachment to Low-LM occurred in the absence of divalent cations, whereas attachment to High-LM required greater than 0.1 mM Ca2+ or Mn2+. Neural crest cell adherence to the E8 fragment of laminin, derived from its long arm, was similar to that on intact laminin at high and low coating concentrations, suggesting that this fragment contains the neural crest cell binding site(s). The HNK-1 antibody recognizes a protein of 165,000 Mr which is also found in immunoprecipitates using antibodies against the beta 1 subunit of integrin and is likely to be an integrin alpha subunit or an integrin-associated protein. Our results suggest that the HNK-1 epitope on neural crest cells is present on or associated with a novel or differentially glycosylated form of beta 1-integrin, which recognizes laminin in the apparent absence of divalent cations. We conclude that neural crest cells have at least two functionally independent means of attachment to laminin which are revealed at different substratum concentrations and/or conformations of laminin.

The differentiation in vitro of the neural crest cells of the mouse embryo

Development ◽  
1984 ◽  
Vol 84 (1) ◽  
pp. 49-62
Author(s):  
Kazuo Ito ◽  
Takuji Takeuchi
Keyword(s):  
Neural Crest ◽  
Mouse Embryo ◽  
Neural Crest Cells ◽  
Culture Method ◽  
Gene Control ◽  
Developmental Potential ◽  
Neural Tubes ◽  
Epithelial Sheet ◽  
Culture Phase

A culture method for neural crest cells of mouse embryo is described. Trunk neural tubes were dissected from 9-day mouse embryos and explanted in culture dishes. The developmental potential of mouse neural crest in vitro was shown to be essentially similar to that of avian neural crest. In the mouse, however, melanocytes always appeared in association with the epithelial sheet close to the explant. Neural crest cells surrounding the epithelial sheet, which probably migrated from the neural tubes in the early culture phase, never differentiated into melanocytes. The bimodal behaviour of mouse crest cells seems to be due to the heterogenous potency of the crest cells and the interaction of these cells with the surrounding microenvironment. This culture system is well suited for various experiments including the analysis of gene control on the differentiation of neural crest cells.

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.

sucker encodes a zebrafish Endothelin-1 required for ventral pharyngeal arch development

Development ◽  
2000 ◽  
Vol 127 (17) ◽  
pp. 3815-3828 ◽  
Author(s):  
C.T. Miller ◽  
T.F. Schilling ◽  
K. Lee ◽  
J. Parker ◽  
C.B. Kimmel
Keyword(s):  
Neural Crest ◽  
Expression Patterns ◽  
Neural Crest Cells ◽  
Paraxial Mesoderm ◽  
Dorsoventral Patterning ◽  
Surface Ectoderm ◽  
Pharyngeal Arches ◽  
Endothelin 1 ◽  
Lower Jaw ◽  
Arch Neural

Mutation of sucker (suc) disrupts development of the lower jaw and other ventral cartilages in pharyngeal segments of the zebrafish head. Our sequencing, cosegregation and rescue results indicate that suc encodes an Endothelin-1 (Et-1). Like mouse and chick Et-1, suc/et-1 is expressed in a central core of arch paraxial mesoderm and in arch epithelia, both surface ectoderm and pharyngeal endoderm, but not in skeletogenic neural crest. Long before chondrogenesis, suc/et-1 mutant embryos have severe defects in ventral arch neural crest expression of dHAND, dlx2, msxE, gsc, dlx3 and EphA3 in the anterior arches. Dorsal expression patterns are unaffected. Later in development, suc/et-1 mutant embryos display defects in mesodermal and endodermal tissues of the pharynx. Ventral premyogenic condensations fail to express myoD, which correlates with a ventral muscle defect. Further, expression of shh in endoderm of the first pharyngeal pouch fails to extend as far laterally as in wild types. We use mosaic analyses to show that suc/et-1 functions nonautonomously in neural crest cells, and is thus required in the environment of postmigratory neural crest cells to specify ventral arch fates. Our mosaic analyses further show that suc/et-1 nonautonomously functions in mesendoderm for ventral arch muscle formation. Collectively our results support a model for dorsoventral patterning of the gnathostome pharyngeal arches in which Et-1 in the environment of the postmigratory cranial neural crest specifies the lower jaw and other ventral arch fates.

Inhibition of noggin expression in the dorsal neural tube by somitogenesis: a mechanism for coordinating the timing of neural crest emigration

Development ◽  
2000 ◽  
Vol 127 (22) ◽  
pp. 4845-4854 ◽  
Author(s):  
D. Sela-Donenfeld ◽  
C. Kalcheim
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Paraxial Mesoderm ◽  
Dorsal Neural Tube ◽  
Progressive Loss ◽  
Crest Cell ◽  
Rostral Part

We have previously shown that axial-dependent delamination of specified neural crest cells is triggered by BMP4 and negatively regulated by noggin. Increasing activity of BMP4 towards the rostral part of the axis is achieved by graded expression of noggin in the dorsal neural tube, the latter being high opposite unsegmented mesoderm, and progressively downregulated facing epithelial and dissociating somites, coinciding in time and axial level with initial delamination of neural crest cells (Sela-Donenfeld, D. and Kalcheim, C. (1999) Development 126, 4749–4762). Here we report that this gradient-like expression of noggin in the neuroepithelium is controlled by the paraxial mesoderm. Deletion of epithelial somites prevented normal downregulation of noggin in the neural tube. Furthermore, partial ablation of either the dorsal half or only the dorsomedial portion of epithelial somites was sufficient to maintain high noggin expression. In contrast, deletion of the segmental plate had no effect. These data suggest that the dorsomedial region of developing somites produces an inhibitor of noggin transcription in the dorsal neural tube. Consistent with this notion, grafting dissociating somites in the place of the unsegmented mesoderm precociously downregulated the expression of noggin and triggered premature emigration of neural crest progenitors from the caudal neural tube. Thus, opposite the unsegmented mesoderm, where noggin expression is high in the neural tube, BMP4 is inactive and neural crest cells fail to delaminate. Upon somitogenesis and further dissociation, the dorsomedial portion of the somite inhibits noggin transcription. Progressive loss of noggin activity releases BMP4 from inhibition, resulting in crest cell emigration. We propose that this inhibitory crosstalk between paraxial mesoderm and neural primordium controls the timing of neural crest delamination to match the development of a suitable mesodermal substrate for subsequent crest migration.

scholarly journals Twist Function Is Required for the Morphogenesis of the Cephalic Neural Tube and the Differentiation of the Cranial Neural Crest Cells in the Mouse Embryo

2002 ◽  
Vol 247 (2) ◽  
pp. 251-270 ◽  
Author(s):  
Kenneth Soo ◽  
Meredith P. O'Rourke ◽  
Poh-Lynn Khoo ◽  
Kirsten A. Steiner ◽  
Nicole Wong ◽  
...  
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Mouse Embryo ◽  
Neural Crest Cells ◽  
Cranial Neural Crest ◽  
Cranial Neural Crest Cells

scholarly journals Neural tube-ectoderm interactions are required for trigeminal placode formation

Development ◽  
1997 ◽  
Vol 124 (21) ◽  
pp. 4287-4295 ◽  
Author(s):  
M.R. Stark ◽  
J. Sechrist ◽  
M. Bronner-Fraser ◽  
C. Marcelle
Keyword(s):  
Neural Crest ◽  
Trigeminal Ganglion ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Surface Ectoderm ◽  
Somite Stage ◽  
Tissue Interactions ◽  
Cranial Neural Crest Cells ◽  
Cranial Sensory Ganglia ◽  
Placode Formation

Cranial sensory ganglia in vertebrates develop from the ectodermal placodes, the neural crest, or both. Although much is known about the neural crest contribution to cranial ganglia, relatively little is known about how placode cells form, invaginate and migrate to their targets. Here, we identify Pax-3 as a molecular marker for placode cells that contribute to the ophthalmic branch of the trigeminal ganglion and use it, in conjunction with DiI labeling of the surface ectoderm, to analyze some of the mechanisms underlying placode development. Pax-3 expression in the ophthalmic placode is observed as early as the 4-somite stage in a narrow band of ectoderm contiguous to the midbrain neural folds. Its expression broadens to a patch of ectoderm adjacent to the midbrain and the rostral hindbrain at the 8- to 10-somite stage. Invagination of the first Pax-3-positive cells begins at the 13-somite stage. Placodal invagination continues through the 35-somite stage, by which time condensation of the trigeminal ganglion has begun. To challenge the normal tissue interactions leading to placode formation, we ablated the cranial neural crest cells or implanted barriers between the neural tube and the ectoderm. Our results demonstrate that, although the presence of neural crest cells is not mandatory for Pax-3 expression in the forming placode, a diffusible signal from the neuroectoderm is required for induction and/or maintenance of the ophthalmic placode.

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