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PubMed1988

Clone-forming ability and differentiation potential of migratory neural crest cells.

The neural crest of vertebrate embryos gives rise to a variety of differentiated cell types, including neuronal and non-neuronal cells of peripheral ganglia (sensory and autonomic), pigment cells, and mesectodermal derivatives. Neural crest cells were taken from quail embryos at the level encompassing mesencephalon and metencephalon and the developmental potentials were evaluated by culturing them as single cells on 3T3 feeder layers. Such conditions proved to be particularly favorable for survival, proliferation, and differentiation of quail neural crest cells. Two hundred and forty-three clones that contained from 1 to greater than 20,000 cells were analyzed after 7-10 days of culture. Phenotype analysis provided evidence for the existence of cells with extremely diverse developmental potencies. A few committed neuron progenitors were observed as well as some pluripotent cells, able to differentiate into several types of neurons, non-neuronal cells, and melanocytes, and many cells with intermediate developmental potencies. These cloning experiments revealed the striking heterogeneity of migrating neural crest cells in terms of their capacity for differentiation and their potential for proliferation.

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PubMed2026

Hox/Meis-dependent gene-regulatory transition underlies cardiopharyngeal neural crest diversification.

Neural crest cells (NCCs) are multipotent migratory cells essential for cardiac development, yet the lineage trajectories and gene regulatory networks underlying their differentiation in the cardiopharyngeal region remain unclear. Here, we integrate single-cell RNA-seq, spatial transcriptomics, and multiomic analyses to construct a comprehensive map of NCC lineages in developing mouse cardiopharyngeal tissues. We identify a transition from Hox-positive pharyngeal NCCs to Hox-negative intracardiac populations associated with the outflow tract cushion, accompanied by a shift in Meis transcription factor binding and gene-regulatory network architecture. By contrast, NCCs forming the aorticopulmonary septum and great vessel smooth muscle retain distinct Hox-codes. A Meis2-Sox9-Scx gene-regulatory network defines a skeletogenic progenitor-like intermediate state that gives rise to coronary artery smooth muscle and semilunar valves. Our findings suggest that the loss of Hox-dependent regional identity enables pharyngeal NCCs to acquire new fates upon entering the cardiac cushion, providing insight into the developmental origins of coronary and valvular calcification.

Journal Article↗
PubMed1978

Effects of mitomycin C in postnatal tooth development in mice with special reference to neural crest cells.

Neural crest cells in the pre- and postnatal development of mice showed a specific sensitivity to mitomycin C. In mice injected with mitomycin C 24-48 h after birth and surviving up to the 9th day, a free or attached denticle in the pulp and a fibroma or excessive cell proliferation in the dental follicle or the periodontal ligament were seen; further, a dentinoma developed.

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PubMed2003

Temporal restriction of migratory and lineage potential in rhombomere 1 and 2 neural crest.

Migratory cranial neural crest cells differentiate into a wide range of cell types, such as ectomesenchymal tissue (bone and connective tissues) ventrally in the branchial arches and neural tissue (neurons and glia) dorsally. We investigated spatial and temporal changes of migration and differentiation potential in neural crest populations derived from caudal midbrain and rhombomeres 1 and 2 by back-transplanting cells destined for the first branchial arch and trigeminal ganglion from HH8-HH19 quail into HH7-HH11 chicks. Branchial arch cells differentiated down ectomesenchymal lineages but largely lost both the ability to localize to the trigeminal position and neurogenic differentiation capacity by HH12-HH13, even before the arch is visible, and lost long distance migratory ability around HH17. In contrast, neural crest-derived cells from trigeminal ganglia lost ectomesechymal differentiation potential by HH17. Despite this, they retain the ability to migrate into the branchial arches until at least HH19. However, many of the neural crest-derived trigeminal ganglia cells in the branchial arch localized to the non-neural crest core of the arch from HH13 and older donors. These results suggest that long distance migration ability, finer scale localization, and lineage restriction may not be coordinately regulated in the cranial neural crest population.

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PubMed2002

Extracellular signals, cell interactions and transcription factors involved in the induction of the neural crest cells.

The neural crest is induced at the border between the neural plate and the epidermis. A complex set of signals is required for the specification of the crest cells between the epidermis and the neural plate. Here we discuss evidence supporting a model for neural crest induction in which different signals contribute in a sequential order. First, a gradient of bone morphogenic proteins (BMPs) is established in the ectoderm that results in segregation into neural plate, neural folds and epidermis at increasing levels of BMP activity. Thus, the neural folds are induced at a precise threshold concentration of BMP, but this neural fold has an anterior character. In a second step, these anterior neural folds are transformed into prospective neural crest by posteriorizing signals due to fibroblast growth factor, Wnts and retinoic acid. Finally, the induced cells interact to complete neural crest induction by a process that requires Notch/Delta signaling. Once neural crest formation has been induced by this combination of extracellular and intracellular signals, a cascade of transcription factors is activated in these cells that culminates in the ultimate steps of neural crest differentiation.

Animals↗
PubMed2000

Fate of the mammalian cardiac neural crest.

A subpopulation of neural crest termed the cardiac neural crest is required in avian embryos to initiate reorganization of the outflow tract of the developing cardiovascular system. In mammalian embryos, it has not been previously experimentally possible to study the long-term fate of this population, although there is strong inference that a similar population exists and is perturbed in a number of genetic and teratogenic contexts. We have employed a two-component genetic system based on Cre/lox recombination to label indelibly the entire mouse neural crest population at the time of its formation, and to detect it at any time thereafter. Labeled cells are detected throughout gestation and in postnatal stages in major tissues that are known or predicted to be derived from neural crest. Labeling is highly specific and highly efficient. In the region of the heart, neural-crest-derived cells surround the pharyngeal arch arteries from the time of their formation and undergo an altered distribution coincident with the reorganization of these vessels. Labeled cells populate the aorticopulmonary septum and conotruncal cushions prior to and during overt septation of the outflow tract, and surround the thymus and thyroid as these organs form. Neural-crest-derived mesenchymal cells are abundantly distributed in midgestation (E9.5-12.5), and adult derivatives of the third, fourth and sixth pharyngeal arch arteries retain a substantial contribution of labeled cells. However, the population of neural-crest-derived cells that infiltrates the conotruncus and which surrounds the noncardiac pharyngeal organs is either overgrown or selectively eliminated as development proceeds, resulting for these tissues in a modest to marginal contribution in late fetal and postnatal life.

Animals↗
PubMed2000

Glial growth factor-2 promotes the survival, migration and bromodeoxyuridine incorporation of mammalian neural crest cells in caudal neural tube explant cultures.

Using an in vitro assay system, we found that GGF-2 increases the number of nascent trunk neural crest cells (NCC) present in the dorsal outgrowth derived from E12 caudal neural tube explants. Data is presented which suggests that this increased outgrowth was due to a combination of GGF-2 mediated effects, including its ability to promote (A) NCC survival by decreasing the percentage of NCC that undergo cell death via a mechanism involving DNA fragmentation, (B) the initial phases of NCC migration, (C) mitosis of peripherally migrating NCC. We also show that GGF-2 can promote the long-term survival of NCC in the absence of the neural tube. An immunohistochemical analysis indicates that NCC express erbB-2 and erbB-4 neuregulin receptors.

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PubMed2003

Xenopus Nbx, a novel NK-1 related gene essential for neural crest formation.

The vertebrate neural crest is formed at the border between the neural plate and nonneural ectoderm during neurulation and eventually gives rise to a variety of cell types, including neurons, glia, facial chondrocytes and osteoblasts, and melanocytes. Although several secreted molecules, such as BMP, Wnts, FGF, and Noelin, have been implicated in neural crest formation, little is known about the precise intracellular mechanism underlying neural crest induction and differentiation. Here, we have identified a novel NK-1 class homeobox gene Nbx in Xenopus whose expression is correlated with neural crest formation. We also found that Nbx harbors an Eh1 domain and is a transcriptional repressor. Overexpression of Nbx suppressed neural plate makers and caused enhanced expression of the neural crest maker Slug. In contrast, the overexpression of a dominant negative form of Nbx during neurula stages suppressed the expression of the neural crest marker Slug and expanded neural markers such as Otx2 and Sox2. Taken together, we propose that Nbx is an essential transcriptional repressor required to permit neural crest induction by inhibiting the neural fate.

Animals↗
PubMed2002

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

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 patterning 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.

Animals↗
PubMed1984

Somatostatin-like immunoreactivity is expressed in neural crest cultures.

Embryonic neural crest cells give rise to many adult cell types, including some neurons that contain the neuroactive peptide somatostatin. The development of somatostatin-like immunoreactive cells has been investigated in quail neural crest cultures. Somatostatin-like immunoreactive cells were first detected in such cultures after 5 days in vitro by immunocytochemistry. The number of immunoreactive cells and the intensity of the immunoreactivity increased dramatically between 5 and 6 days in vitro. The immunoreactivity was present in a small subset of cells in the culture. It was seen in the perikaryon and cellular processes, but was absent from the nucleus. Immunoreactive cells with and without processes were observed. Somatostatin immunoreactivity was absent if the anti-somatostatin serum was preincubated in the presence of somatostatin. A sequential procedure for detecting catecholamine-containing cells histochemically followed by immunocytochemistry for somatostatin-like immunoreactivity showed that about 20% of the cells which contained catecholamines also contained somatostatin-like immunoreactivity. Greater than 90% of the somatostatin-containing cells in this analysis also contained catecholamines. Somatostatin-like immunoreactivity was also detected and quantitated by radioimmunoassay. The somatostatin-like immunoreactivity developed in vitro in medium that contained horse serum and chick embryo extract, but in the absence of other embryonic cell types such as notochord and somitic mesenchyme. These in vitro results together with prior in vivo data indicate that expression of somatostatin-like immunoreactivity is an early event in the development of some neural crest cells which also express adrenergic properties.

Animals↗
PubMed2004

Long-distance cue from emerging dermis stimulates neural crest melanoblast migration.

Neural crest melanoblasts display unique navigational abilities enabling them to colonize the dorsal path between ectoderm and somite. One signal shown here to elicit melanoblast migration is a chemotactic cue supplied by the emerging dermis. Until dermis emerges, melanoblasts fail to enter the dorsal path. The dermis emerges from a site that is too distant to stimulate migration by cell contact. Instead, surgeries show that dermis elicits migration from a distance. When dermis is grafted distally, neural crest cells enter the path precociously. Moreover, large grafts recruit melanoblasts from the control sides (without increasing crest cell numbers) as well as a few crest cells from ventral somite. Because other grafted tissues fail to stimulate migration, the dermis stimulus is specific. This report is the first documentation that trunk neural crest cells can be guided chemotactically. It also extends evidence that migration is exquisitely sensitive to temporal-spatial patterns of somite morphogenesis. Developmental Dynamics 229:99-108, 2004.

Animals↗
PubMed2001

The winged-helix transcription factor Foxd3 suppresses interneuron differentiation and promotes neural crest cell fate.

The neural crest is a migratory cell population that gives rise to multiple cell types in the vertebrate embryo. The intrinsic determinants that segregate neural crest cells from multipotential dorsal progenitors within the neural tube are poorly defined. In this study, we show that the winged helix transcription factor Foxd3 is expressed in both premigratory and migratory neural crest cells. Foxd3 is genetically downstream of Pax3 and is not expressed in regions of Pax3 mutant mice that lack neural crest, implying that Foxd3 may regulate aspects of the neural crest differentiation program. We show that misexpression of Foxd3 in the chick neural tube promotes a neural crest-like phenotype and suppresses interneuron differentiation. Cells that ectopically express Foxd3 upregulate HNK1 and Cad7, delaminate and emigrate from the neural tube at multiple dorsoventral levels. Foxd3 does not induce Slug and RhoB, nor is its ability to promote a neural crest-like phenotype enhanced by co-expression of Slug. Together these results suggest Foxd3 can function independently of Slug and RhoB to promote the development of neural crest cells from neural tube progenitors.

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PubMed1993

Origins of neural crest cell diversity.

The neural crest is a population of migratory cells, arising from the ectoderm, that invades many sites within the embryo and differentiate into a variety of diverse cell types. Pigment cells, most cells of the peripheral nervous system, adrenal medullary cells, and some cranial cartilage are derived from the neural crest. Despite a wealth of knowledge concerning their pathways of migration and vast array of derivatives, little is known about the formation of neural crest cells or their acquisition of positional identity. This review focuses on the origin of neural crest cells from the ectoderm and the generation of differences in neural crest cell fates along the rostrocaudal axis. In addition, we consider the role of temporal restriction in the developmental potential of premigratory neural crest cells. While evidence for the existence of multipotent stem cells is strong, some experiments also suggest that there may be heterogeneity among neural crest cell precursors, perhaps due to differences in origin, that might explain commitment events occurring early in neural crest development.

Animals↗
PubMed1987

Cell lineages in peripheral nervous system ontogeny: medium-induced modulation of neuronal phenotypic expression in neural crest cell cultures.

Neural crest, taken from cephalic and trunk levels of quail embryos, was grown in vitro in conventional tissue culture medium (Dulbecco's modified Eagle's medium containing 15% fetal calf serum and either 2 or 15% chick embryo extract (CEE] or in a chemically defined serum- and CEE-free medium. Depending on the conditions employed, different types of neuronal or neuronlike cells developed in the cultures. Thus, in medium containing 15% CEE, adrenergic cells (identified by tyrosine hydroxylase immunoreactivity and catecholamine histofluorescence) emerged after 5-6 days. These cells lacked tetanus toxin binding sites and did not react with an antibody directed against 70-kDa neurofilament protein. In the fully defined medium, a neuronal cell type exhibiting neurofilament and substance P (SP) immunoreactivity differentiated from noncycling precursors within 1 or 2 days of culture. If serum was added to the medium, the neurites disintegrated and the neuronal cells ultimately died. By sequentially culturing neural crest, first in the wholly synthetic medium for 1-3 days and then in the conventional medium supplemented with serum and 15% CEE, the disappearance of the SP-positive neurons was followed, several days later, by the emergence of adrenergic cells. The majority of these cells and/or their precursors were found to undergo cell division in culture. We conclude that the cells expressing the adrenergic phenotype (characteristic of the sympathetic nervous system) and those displaying SP immunoreactivity, comparable to a category of neurons in dorsal root and cranial sensory ganglia, derive from distinct sets of precursors. Our results reinforce the contention, deduced from in ovo transplantation experiments (see N. M. Le Douarin, (1984) In Cellular and Molecular Biology of Neuronal Development (I. Black, Ed.), pp. 3-28. Plenum, New York), that at least two lineages, from which sensory and autonomic cell types are derived respectively, are segregated early during neural crest ontogeny and have extremely different survival and trophic requirements.

Acetylcholine↗
PubMed2000

In ovo time-lapse analysis after dorsal neural tube ablation shows rerouting of chick hindbrain neural crest.

Previous analyses of single neural crest cell trajectories have suggested important roles for interactions between neural crest cells and the environment, and amongst neural crest cells. To test the relative contribution of intrinsic versus extrinsic information in guiding cells to their appropriate sites, we ablated subpopulations of premigratory chick hindbrain neural crest and followed the remaining neural crest cells over time using a new in ovo imaging technique. Neural crest cell migratory behaviors are dramatically different in ablated compared with unoperated embryos. Deviations from normal migration appear either shortly after cells emerge from the neural tube or en route to the branchial arches, areas where cell-cell interactions typically occur between neural crest cells in normal embryos. Unlike the persistent, directed trajectories in normal embryos, neural crest cells frequently change direction and move somewhat chaotically after ablation. In addition, the migration of neural crest cells in collective chains, commonly observed in normal embryos, was severely disrupted. Hindbrain neural crest cells have the capacity to reroute their migratory pathways and thus compensate for missing neural crest cells after ablation of neighboring populations. Because the alterations in neural crest cell migration are most dramatic in regions that would normally foster cell-cell interactions, the trajectories reported here argue that cell-cell interactions have a key role in the shaping of the neural crest migration.

Animals↗
PubMed2000

Delta signaling mediates segregation of neural crest and spinal sensory neurons from zebrafish lateral neural plate.

We examined the role of Delta signaling in specification of two derivatives in zebrafish neural plate: Rohon-Beard spinal sensory neurons and neural crest. deltaA-expressing Rohon-Beard neurons are intermingled with premigratory neural crest cells in the trunk lateral neural plate. Embryos homozygous for a point mutation in deltaA, or with experimentally reduced delta signalling, have supernumerary Rohon-Beard neurons, reduced trunk-level expression of neural crest markers and lack trunk neural crest derivatives. Fin mesenchyme, a putative trunk neural crest derivative, is present in deltaA mutants, suggesting it segregates from other neural crest derivatives as early as the neural plate stage. Cranial neural crest derivatives are also present in deltaA mutants, revealing a genetic difference in regulation of trunk and cranial neural crest development.

Animals↗
PubMed1995

Patterning of the vertebrate neural crest.

The mechanisms underlying neural crest cell migration are beginning to be understood thanks to the ability to combine a number of techniques in experimental embryology, cell and molecular biology. In the trunk, cell-cell interactions may predominate, so that the mesodermal somites control the rostrocaudal patterning of neural crest cells and the notochord prevents neural crest cells from crossing the midline. In the hindbrain, the segmental migration of neural crest cells may be influenced both by information inherent to the rhombomeres coupled with environmental signals from neighboring tissues, such as the otic vesicle. There is clearly an intimate relationship between migrating neural crest cells, the neural tube from which they emerge, and tissues through which they move. All of these elements are integral in the control of neural crest migration.

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