Distribution and migration pathways of HNK-1-immunoreactive neural crest cells in teleost fish embryos

Development ◽  
1990 ◽  
Vol 110 (1) ◽  
pp. 197-209
Author(s):  
B. Sadaghiani ◽  
J.R. Vielkind
Keyword(s):  
Neural Crest ◽  
Cross Sections ◽  
Teleost Fish ◽  
Sensory System ◽  
Neural Crest Cells ◽  
Similar Distribution ◽  
Major Pathway ◽  
Anterior Trunk ◽  
And Migration ◽  
Migration Pathways

Whole mounts and cross-sections of embryos from three species of teleost fish were immunostained with the HNK-1 monoclonal antibody, which recognizes an epitope on migrating neural crest cells. A similar distribution and migration was found in all three species. The crest cells in the head express the HNK-1 epitope after they have segregated from the neural keel. The truncal neural crest cells begin to express the epitope while they still reside in the dorsal region of the neural keel; this has not been observed in other vertebrates. The cephalic and anterior truncal neural crest cells migrate under the ectoderm; the cephalic cells then enter into the gill arches and the anterior truncal cells into the mesentery of the digestive tract where they cease migration. These cephalic and anterior trunk pathways are similar to those described in Xenopus and chick. The neural crest cells of the trunk, after segregation, accumulate in the dorsal wedges between the somites, however, unlike in chick and rat, they do not migrate in the anterior halves of the somites but predominantly between the neural tube and the somites, the major pathway observed in carp and amphibians; some cells migrate over the somites. The HNK-1 staining of whole-mount embryos revealed a structure resembling the Rohon-Beard and extramedullary cells, the primary sensory system in amphibians. Such a system has not been described in fish.

Signalling between the hindbrain and paraxial tissues dictates neural crest migration pathways

Development ◽  
2002 ◽  
Vol 129 (2) ◽  
pp. 433-442 ◽  
Author(s):  
Paul A. Trainor ◽  
Dorothy Sobieszczuk ◽  
David Wilkinson ◽  
Robb Krumlauf
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Cranial Neural Crest ◽  
Branchial Arches ◽  
Neural Crest Cell Migration ◽  
And Migration ◽  
Migration Pathways ◽  
Crest Cell

Cranial neural crest cells are a pluripotent population of cells derived from the neural tube that migrate into the branchial arches to generate the distinctive bone, connective tissue and peripheral nervous system components characteristic of the vertebrate head. The highly conserved segmental organisation of the vertebrate hindbrain plays an important role in pattering the pathways of neural crest cell migration and in generating the distinct or separate streams of crest cells that form unique structures in each arch. We have used focal injections of DiI into the developing mouse hindbrain in combination with in vitro whole embryo culture to map the patterns of cranial neural crest cell migration into the developing branchial arches. Our results show that mouse hindbrain-derived neural crest cells migrate in three segregated streams adjacent to the even-numbered rhombomeres into the branchial arches, and each stream contains contributions of cells from three rhombomeres in a pattern very similar to that observed in the chick embryo. There are clear neural crest-free zones adjacent to r3 and r5. Furthermore, using grafting and lineage-tracing techniques in cultured mouse embryos to investigate the differential ability of odd and even-numbered segments to generate neural crest cells, we find that odd and even segments have an intrinsic ability to produce equivalent numbers of neural crest cells. This implies that inter-rhombomeric signalling is less important than combinatorial interactions between the hindbrain and the adjacent arch environment in specific regions, in the process of restricting the generation and migration of neural crest cells. This creates crest-free territories and suggests that tissue interactions established during development and patterning of the branchial arches may set up signals that the neural plate is primed to interpret during the progressive events leading to the delamination and migration of neural crest cells. Using interspecies grafting experiments between mouse and chick embryos, we have shown that this process forms part of a conserved mechanism for generating neural crest-free zones and contributing to the separation of migrating crest populations with distinct Hox expression during vertebrate head development.

Changes in the distribution of extracellular matrix components during neural crest development in Xiphophorus spp. embryos

1994 ◽  
Vol 72 (7) ◽  
pp. 1340-1353 ◽  
Author(s):  
Bahram Sadaghiani ◽  
Bruce J. Crawford ◽  
Juergen R. Vielkind
Keyword(s):  
Extracellular Matrix ◽  
Neural Crest ◽  
Critical Role ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Weak Staining ◽  
Extracellular Matrix Components ◽  
Neural Crest Cell Migration ◽  
And Migration ◽  
Migration Pathways

The changes in distribution of chondroitin sulfate proteoglycans (CSs) and fibronectin (FN), two major components of the extracellular matrix (ECM), are described during the development and migration of neural crest cells in two Xiphophorus species offish, X. helleri (swordtail) and X. maculatus (platyfish), using immunohistochemistry. A detailed description of the developmental changes in HNK-1-positive ECM components is also provided and compared with those of CSs and FN. HNK-1 antigen was also used as a marker for the neural crest cells. Weak staining for CSs, FN, and HNK-1-positive ECM was present in the neural crest cell migration pathways prior to migration of the cells. The level of staining increased dramatically during migration of these cells and decreased again after migration was nearly completed. Staining for CSs was more widespread than staining for FN, while the HNK-1 staining pattern was more clearly restricted to the migratory pathways than those seen with the other two antibodies. The correlation between the spatiotemporal relationship of these ECM components and the segregation and migration of neural crest cells suggests that these ECM molecules may be involved in both initiating and guiding the migration of neural crest cells in these fish. The HNK-1-positive ECM may play a more critical role than CSs and FN.

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

Development ◽  
1999 ◽  
Vol 126 (10) ◽  
pp. 2181-2189 ◽  
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.

scholarly journals Neural crest cell migration: requirements for exogenous fibronectin and high cell density.

1983 ◽  
Vol 96 (2) ◽  
pp. 462-473 ◽  
Author(s):  
R A Rovasio ◽  
A Delouvee ◽  
K M Yamada ◽  
R Timpl ◽  
J P Thiery
Keyword(s):  
Cell Adhesion ◽  
Neural Crest ◽  
Type I Collagen ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Type I ◽  
Cell Adhesion And Migration ◽  
And Migration ◽  
Crest Cell

Cells of the neural crest participate in a major class of cell migratory events during embryonic development. From indirect evidence, it has been suggested that fibronectin (FN) might be involved in these events. We have directly tested the role of FN in neural crest cell adhesion and migration using several in vitro model systems. Avian trunk neural crest cells adhered readily to purified plasma FN substrates and to extracellular matrices containing cellular FN. Their adhesion was inhibited by antibodies to a cell-binding fragment of FN. In contrast, these cells did not adhere to glass, type I collagen, or to bovine serum albumin in the absence of FN. Neural crest cell adhesion to laminin (LN) was significantly less than to FN; however, culturing of crest cells under conditions producing an epithelioid phenotype resulted in cells that could bind equally as well to LN as to FN. The migration of neural crest cells appeared to depend on both the substrate and the extent of cell interactions. Cells migrated substantially more rapidly on FN than on LN or type I collagen substrates; if provided a choice between stripes of FN and glass or LN, cells migrated preferentially on the FN. Migration was inhibited by antibodies against the cell-binding region of FN, and the inhibition could be reversed by a subsequent addition of exogenous FN. However, the migration on FN was random and displayed little persistence of direction unless cells were at high densities that permitted frequent contacts. The in vitro rate of migration of cells on FN-containing matrices was 50 microns/h, similar to their migration rates along the narrow regions of FN-containing extracellular matrix in migratory pathways in vivo. These results indicate that FN is important for neural crest cell adhesion and migration and that the high cell densities of neural crest cells in the transient, narrow migratory pathways found in the embryo are necessary for effective directional migration.

Fibronectin Combined with Stem Cell Factor Plays an Important Role in Melanocyte Proliferation, Differentiation and Migration in Cultured Mouse Neural Crest Cells

2002 ◽  
Vol 15 (3) ◽  
pp. 192-200 ◽  
Author(s):  
Nagako Takano ◽  
Tamihiro Kawakami ◽  
Yoko Kawa ◽  
Mari Asano ◽  
Hidenori Watabe ◽  
...  
Keyword(s):  
Stem Cell ◽  
Neural Crest ◽  
Stem Cell Factor ◽  
Neural Crest Cells ◽  
And Migration

Dissociation and Reaggregation of Embryonic cells of Triturus alpestris

Development ◽  
1955 ◽  
Vol 3 (3) ◽  
pp. 251-255
Author(s):  
M. Feldman
Keyword(s):  
Embryonic Development ◽  
Neural Crest ◽  
Cell Movement ◽  
Neural Crest Cells ◽  
Embryonic Cells ◽  
Experimental Conditions ◽  
Developmental Processes ◽  
Triturus Alpestris ◽  
And Migration

Cell movement and migration seem to play an important role in the formation of tissue-patterns during embryogenesis. Phenomena such as the appearance of loosely attached cells in the mesoderm, or of the freely migrating neural crest cells, are quite common in embryonic development. Since the tissues of adult organs are mostly rather compact in structure it seems that the capacity of isolated or loosely arranged cells to reassociate is an obligatory condition for many developmental processes. This capacity, under experimental conditions, was extensively studied by Holtfreter (1947, 1948). He has shown that cells of newt blastulae and early gastrulae can be made to dissociate and can then become reaggregated and proceed with their morphogenetic development. His experiments were carried out, for the most part, either with cells prior to histogenetic determination or with determined cells of a single tissue.

scholarly journals BMP-switching regulates lineage specification and migration of neural crest cells

2010 ◽  
Vol 344 (1) ◽  
pp. 473
Author(s):  
Daisuke Saito ◽  
Emi Ohata ◽  
Hidetaka Murai ◽  
Yuta Takase ◽  
Yoshiko Takahashi
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Lineage Specification ◽  
And Migration

scholarly journals Sonic hedgehog restricts adhesion and migration of neural crest cells independently of the Patched- Smoothened-Gli signaling pathway

2001 ◽  
Vol 98 (22) ◽  
pp. 12521-12526 ◽  
Author(s):  
S. Testaz ◽  
A. Jarov ◽  
K. P. Williams ◽  
L. E. Ling ◽  
V. E. Koteliansky ◽  
...  
Keyword(s):  
Neural Crest ◽  
Signaling Pathway ◽  
Sonic Hedgehog ◽  
Neural Crest Cells ◽  
And Migration

scholarly journals AKT Signaling Modifies the Balance between Cell Proliferation and Migration in Neural Crest Cells from Patients Affected with Bosma Arhinia and Microphthalmia Syndrome

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 751
Author(s):  
Camille Laberthonnière ◽  
Elva Maria Novoa-del-Toro ◽  
Raphaël Chevalier ◽  
Natacha Broucqsault ◽  
Vanitha Venkoba Rao ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Neural Crest ◽  
Differential Expression ◽  
Biological Networks ◽  
Neural Crest Cells ◽  
Akt Signaling ◽  
Hormone Deficiency ◽  
Pituitary Hormone ◽  
And Migration

Over the recent years, the SMCHD1 (Structural Maintenance of Chromosome flexible Hinge Domain Containing 1) chromatin-associated factor has triggered increasing interest after the identification of variants in three rare and unrelated diseases, type 2 Facio Scapulo Humeral Dystrophy (FSHD2), Bosma Arhinia and Microphthalmia Syndrome (BAMS), and the more recently isolated hypogonadotrophic hypogonadism (IHH) combined pituitary hormone deficiency (CPHD) and septo-optic dysplasia (SOD). However, it remains unclear why certain mutations lead to a specific muscle defect in FSHD while other are associated with severe congenital anomalies. To gain further insights into the specificity of SMCHD1 variants and identify pathways associated with the BAMS phenotype and related neural crest defects, we derived induced pluripotent stem cells from patients carrying a mutation in this gene. We differentiated these cells in neural crest stem cells and analyzed their transcriptome by RNA-Seq. Besides classical differential expression analyses, we analyzed our data using MOGAMUN, an algorithm allowing the extraction of active modules by integrating differential expression data with biological networks. We found that in BAMS neural crest cells, all subnetworks that are associated with differentially expressed genes converge toward a predominant role for AKT signaling in the control of the cell proliferation–migration balance. Our findings provide further insights into the distinct mechanism by which defects in neural crest migration might contribute to the craniofacial anomalies in BAMS.

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