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PubMed2004

Cell surface molecules and truncal neural crest ontogeny: a perspective.

The neural crest cell is synonymous with vertebrates and can be viewed as a transitory, mobile vector that conveys neuroepithelial stem cells to a diverse number of remote locations in the embryo. Neural crest cells have been studied intensively over the past 30 years, and it is increasingly apparent that their fate is, at least in part, directed extrinsically by the environment to which they are exposed in vivo. The interface between the cell surface and the opposing environment is clearly an important compartment for the correct deployment of the neural crest. Here, we review some of the molecules present in this location and how they influence the fate of the neural crest and generate disease.

Animals↗
PubMed2006

An in vitro model for characterizing the post-migratory cranial neural crest cells of the first branchial arch.

The cranial neural crest (CNC) is a transient cell population that originates at the crest of the neural fold and gives rise to multiple cell types during craniofacial development. Traditionally, researchers have used tissue explants, such as the neural tube, to obtain primary neural crest cells for their studies. However, this approach has inevitably resulted in simultaneous isolation of neural and non-neural crest cells as both of these cells migrate away from tissue explants. Using the Wnt1-Cre/R26R mouse model, we have obtained a pure population of neural crest cells and established a primary CNC cell culture system in which the cell culture medium best supports the proliferation of E10.5 first branchial arch CNC cells and maintains these cells in their undifferentiated state. Differentiation of CNC cells can be initiated by switching to a differentiation medium. In this model, cultured CNC cells can give rise to neurons, glial cells, osteoblasts, and other cell types, faithfully mimicking the differentiation process of the post-migratory CNC cells in vivo. Taken together, our study shows that the Wnt1-Cre/R26R mouse first branchial arch provides an excellent model for obtaining post-migratory neural crest cells free of any mesodermal contaminants. The cultured neural crest cells are under sustained proliferative, undifferentiated, or lineage-enhanced conditions, hence, serving as a tool for the investigation of the regulatory mechanism of CNC cell fate determination in normal and abnormal craniofacial development.

Animals↗
PubMed1996

The regeneration of the cephalic neural crest, a problem revisited: the regenerating cells originate from the contralateral or from the anterior and posterior neural fold.

The mesencephalic and rhombencephalic levels of origin of the hypobranchial skeleton (lower jaw and hyoid bone) within the neural fold have been determined at the 5-somite stage with a resolution corresponding to each single rhombomere, by means of the quail-chick chimera technique. Expression of certain Hox genes (Hoxa-2, Hoxa-3 and Hoxb-4) was recorded in the branchial arches of chick and quail embryos at embryonic days 3 (E3) and E4. This was a prerequisite for studying the regeneration capacities of the neural crest, after the dorsal neural tube was resected at the mesencephalic and rhombencephalic level. We found first that excisions at the 5-somite stage extending from the midmesencephalon down to r8 are followed by the regeneration of neural crest cells able to compensate for the deficiencies so produced. This confirmed the results of previous authors who made similar excisions at comparable (or older) developmental stages. When a bilateral excision was followed by the unilateral homotopic graft of the dorsal neural tube from a quail embryo, thus mimicking the situation created by a unilateral excision, we found that the migration of the grafted unilateral neural crest (quail-labelled) is bilateral and compensates massively for the missing crest derivatives. The capacity of the intermediate and ventral neural tube to yield neural crest cells was tested by removing the chick rhombencephalic neural tube and replacing it either uni- or bilaterally with a ventral tube coming from a stage-matched quail. No neural crest cells exited from the ventral neural tube but no deficiency in neural crest derivatives was recorded. Crest cells were found to regenerate from the ends of the operated region. This was demonstrated by grafting fragments of quail neural fold at the extremities of the excised territory. Quail neural crest cells were seen migrating longitudinally from both the rostral and caudal ends of the operated region and filling the branchial arches located inbetween. Comparison of the behaviour of neural crest cells in this experimental situation with that showed by their normal fate map revealed that crest cells increase their proliferation rate and change their migratory behaviour without modifying their Hox code.

Animals↗
PubMed1996

Multiple actions of stem cell factor in neural crest cell differentiation in vitro.

The neural crest is a transient tissue of the vertebrate embryo that gives rise to most primary sensory neurons and pigment cells in the adult organism, among other cell types and tissues. Many neural crest cells are pluripotent in the sense that their progeny can generate more than one phenotype. The presence of pluripotent neural crest cell-derived cells at sites of terminal differentiation suggests that location-specific cues from the embryonic environment, such as growth factors, are involved in directing their survival, proliferation, and cell type specification. We have therefore examined the influences of one pertinent growth factor, stem cell factor (SCF), on neural crest cell development by in vitro colony assay in a serum-free culture medium. SCF showed three major effects. (1) SCF is trophic for early neural crest cells, that is, either pluripotent cells and/or their more mature progeny. This effect occurs only if SCF is present throughout the culture period, and it is not observed when a neurotrophin is present in addition to SCF. (2) More colonies contain sensory neuron precursors in the presence of SCF. This effect is neutralized by NGF and neurotrophin-3 (NT-3), but not by brain-derived neurotrophic factor (BDNF). (3) The combination of SCF and any neurotrophin tested (NGF, BDNF, NT-3) is trophic for melanogenic cells, whereas SCF alone does not detectably affect melanogenesis. This suggests either that both types of factor are required for melanotrophic action or that melanogenic cells become dependent on neurotrophins after exposure to SCF. Our observation that SCF is required during the first half of the culture period only, and NGF during the second half only, indicates the latter possibility. Whereas coat color changes in the mouse mutants W (c-kit defect) and Steel (SCF defect) and several in vivo and in vitro studies by other investigators have shown previously that SCF is melanotrophic, they also indicated the requirement of an additional factor, or factors, in melanogenesis. Our data suggest that SCF affects neural crest cell development at multiple levels and that survival of melanogenic cells is mediated by a combination of SCF and a neurotropin, rather than by SCF alone.

Animals↗
PubMed1987

Melanocyte-stimulating hormone affects melanogenic differentiation of quail neural crest cells in vitro.

Quail neural crest cells were treated in vitro with alpha-melanocyte-stimulating hormone (alpha-MSH) or dibutyryl cyclic AMP (dbcAMP) plus theophylline. These treatments increased the proportion of melanocytes to total cells in crest cell outgrowth cultures. Pigmentation of neural crest cell clusters proceeded more rapidly when cultures were treated with alpha-MSH or dbcAMP plus theophylline than when untreated. In clonal cell cultures, the proportion of pigmented colonies to total colonies was increased by MSH treatment. From these results, MSH seems not only to accelerate melanogenic differentiation but also to affect the state of commitment of neural crest cells to melanogenic differentiation in vitro, and this action of MSH appears to be mediated by cAMP.

Animals↗
PubMed2002

An amphioxus winged helix/forkhead gene, AmphiFoxD: insights into vertebrate neural crest evolution.

During amphioxus development, the neural plate is bordered by cells expressing many genes with homologs involved in vertebrate neural crest induction. However, these amphioxus cells evidently lack additional genetic programs for the cell delaminations, migrations, and differentiations characterizing definitive vertebrate neural crest. We characterize an amphioxus winged helix/forkhead gene (AmphiFoxD) closely related to vertebrate FoxD genes. Phylogenetic analysis indicates that the AmphiFoxD is basal to vertebrate FoxD1, FoxD2, FoxD3, FoxD4, and FoxD5. One of these vertebrate genes (FoxD3) consistently marks neural crest during development. Early in amphioxus development, AmphiFoxD is expressed medially in the anterior neural plate as well as in axial (notochordal) and paraxial mesoderm; later, the gene is expressed in the somites, notochord, cerebral vesicle (diencephalon), and hindgut endoderm. However, there is never any expression in cells bordering the neural plate. We speculate that an AmphiFoxD homolog in the common ancestor of amphioxus and vertebrates was involved in histogenic processes in the mesoderm (evagination and delamination of the somites and notochord); then, in the early vertebrates, descendant paralogs of this gene began functioning in the presumptive neural crest bordering the neural plate to help make possible the delaminations and cell migrations that characterize definitive vertebrate neural crest.

Animals↗
PubMed2006

Conserved RARE localization in amphioxus Hox clusters and implications for Hox code evolution in the vertebrate neural crest.

The Hox code in the neural crest cells plays an important role in the development of the complex craniofacial structures that are characteristic of vertebrates. Previously, 3' AmphiHox1 flanking region has been shown to drive gene expression in neural tubes and neural crest cells in a retinoic acid (RA)-dependent manner. In the present study, we found that the DR5-type RA response elements located at the 3' AmphiHox1 flanking region of Branchiostoma floridae are necessary and sufficient to express reporter genes in both the neural tube and neural crest cells of chick embryos, specifically at the post-otic level. The DR5 at the 3' flanking region of chick Hoxb1 is also capable of driving the same expression in chick embryos. We found that AmphiHox3 possesses a DR5-type RARE in its 5' flanking region, and this drives an expression pattern similar to the RARE element found in the 3' flanking region of AmphiHox1. Therefore, the location of these DR5-type RAREs is conserved in amphioxus and vertebrate Hox clusters. Our findings demonstrate that conserved RAREs mediate RA-dependent regulation of Hox genes in amphioxus and vertebrates, and in vertebrates this drives expression of Hox genes in both neural crest and neural tube. This suggests that Hox expression in vertebrate neural crest cells has evolved via the co-option of a pre-existing regulatory pathway that primitively regulated neural tube (and possibly epidermal) Hox expression.

Animals↗
PubMed1994

Neural crest cell formation and migration in the developing embryo.

Neural crest cells arise from the neural tube shortly after its closure and migrate extensively through prescribed regions of the embryos, where they differentiate into most of the peripheral nervous system as well as the facial skeleton and pigment cells. Along the embryonic axis, several distinct neural crest populations differ both in their migratory pathways and range of derivatives. Whereas those cells arising from the midbrain migrate as a uniform sheet of cells, neural crest cells emerging from the hindbrain and trunk regions migrate in a segmented manner. For example, trunk neural crest cells move preferentially through the rostral, but not caudal, half of each somite. Interactions with tissues encountered during migration strongly influence this segmental migratory pattern. For example, the mesodermal somites dictate the segmental migration of trunk neural crest cells and the otic placode appears to attract hindbrain neural crest cells. Although little is known about the molecular basis underlying migration, patterns of gene expression in the hindbrain are thought to contribute to the segmental arrangement of neural crest cells. Furthermore, neural crest cells possess integrin receptors that may be important for interacting with extracellular matrix molecules in their surroundings.

Cell Movement↗
PubMed1997

Interactions of Eph-related receptors and ligands confer rostrocaudal pattern to trunk neural crest migration.

BACKGROUND: In the trunk of avian embryos, neural crest migration through the somites is segmental, with neural crest cells entering the rostral half of each somitic sclerotome but avoiding the caudal half. Little is known about the molecular nature of the cues-intrinsic to the somites-that are responsible for this segmental migration of neural crest cells. RESULTS: We demonstrate that Eph-related receptor tyrosine kinases and their ligands are essential for the segmental migration of avian trunk neural crest cells through the somites. EphB3 localizes to the rostral half-sclerotome, including the neural crest, and the ligand ephrin-B1 has a complementary pattern of expression in the caudal half-sclerotome. To test the functional significance of this striking asymmetry, soluble ligand ephrin-B1 was added to interfere with receptor function in either whole trunk explants or neural crest cells cultured on alternating stripes of ephrin-B1 versus fibronection. Neural crest cells in vitro avoided migrating on lanes of immobilized ephrin-B1; the addition of soluble ephrin-B1 blocked this inhibition. Similarly, in whole trunk explants, the metameric pattern of neural crest migration was disrupted by addition of soluble ephrin-B1, allowing entry of neural crest cells into caudal portions of the sclerotome. CONCLUSIONS: Both in vivo and in vitro, the addition of soluble ephrin-B1 results in a loss of the metameric migratory pattern and a disorganization of neural crest cell movement. These results demonstrate that Eph-family receptor tyrosine kinases and their transmembrane ligands are involved in interactions between neural crest and sclerotomal cells, mediating an inhibitory activity necessary to constrain neural precursors to specific territories in the developing nervous system.

Animals↗
PubMed2005

Neural crest induction by the canonical Wnt pathway can be dissociated from anterior-posterior neural patterning in Xenopus.

While Wnt signaling is known to be involved in early steps of neural crest development, the mechanism remains unclear. Because Wnt signaling is able to posteriorize anterior neural tissues, neural crest induction by Wnts has been proposed to be an indirect consequence of posteriorization of neural tissues rather than a direct effect of Wnt signaling. To address the relationship between posteriorization and neural crest induction by Wnt signaling, we have used gain of function and loss of function approaches in Xenopus to modulate the level of Wnt signaling at multiple points in the pathway. We find that modulating the level of Wnt signaling allows separation of neural crest induction from the effects of Wnts on anterior-posterior neural patterning. We also find that activation of Wnt signaling induces ectopic neural crest in the anterior region without posteriorizing anterior neural tissues. In addition, Wnt signaling induces neural crest when its posteriorizing activity is blocked by inhibition of FGF signaling in neuralized explants. Finally, depletion of beta-catenin confirms that the canonical Wnt pathway is required for initial neural crest induction. While these observations do not exclude a role for posteriorizing signals in neural crest induction, our data, together with previous observations, strongly suggest that canonical Wnt signaling plays an essential and direct role in neural crest induction.

Animals↗
PubMed1996

Contact inhibition/collapse and pathfinding of neural crest cells in the zebrafish trunk.

Neural crest cells in the trunk of vertebrate embryos have a choice of pathways after emigrating from the neural tube: they can migrate in either the medial pathway between somites and neural tube, or the lateral pathway between somites and epidermis. In zebrafish embryos, the first cells to migrate all choose the medial pathway. High resolution imaging of cells in living embryos suggests that neural crest cells do so because of repulsion by somites: cells take the medial pathway because the lateral somite surface triggers a paralysis and retraction of protrusions (contact inhibition or collapse) when the medial surface does not. Partial deletion of somites, using the spadetail mutation allows precocious entry into the lateral pathway, but only where somites are absent, supporting the notion that an inhibitory cue on somites delays entry. Growth cones of Rohon-Beard cells enter the lateral pathway before neural crest cells, demonstrating that there is no absolute barrier to migration. These data, in addition to providing a detailed picture of neural crest cells migrating in vivo, suggest that neural crest cells, like neuronal growth cones, are guided by a specific cue that triggers 'collapse' of active protrusions.

Animals↗
PubMed1995

Retinoic acid promotes the differentiation of adrenergic cells and melanocytes in quail neural crest cultures.

The neural crest (NC) generates very diverse neuronal and nonneuronal cell types in the vertebrate embryo. Pluripotency and plasticity of NC cells have been demonstrated, but the mechanisms whereby extrinsic factors control NC cell diversification are still unknown. Here we have investigated in vitro the influence of the morphogen retinoic acid (RA) in cultures of quail NC cells explanted at different developmental stages, when they start to migrate from the neural primordium, and when they reach their target organs. We found that addition of RA to mass cultures of early-migrating trunk NC promotes the differentiation of melanocytes and adrenergic cells. These responses are dose-dependent and vary according to the time of RA exposure. Testing RA effect on crest-derived cells located in Embryonic Day 3 (E3) somites and in E4 skin showed that the adrenergic-promoting action of RA is restricted to early-migratory cells, while melanogenic precursors colonizing the skin remain sensitive to RA for a longer period. Furthermore, analysis of cephalic and trunk NC clonal cultures revealed that RA influences the differentiation of cells when they are in a pluripotent state: among the progeny of isolated crest cells, RA specifically increases the number of the adrenergic cells, very likely by influencing their commitment; moreover, RA stimulates pigment synthesis in the melanoblasts. In conclusion, these results demonstrate that RA enhances in vitro the differentiation of NC cells and support a role for endogenous retinoids in the ontogeny of NC derivatives.

Adrenergic Fibers↗
PubMed1985

Appearance of nerve growth factor receptors on cultured neural crest cells.

Light microscopic radioautography of differentiating quail neural crest cultures (1 to 2 weeks after explanation) incubated with Iodine-125-labeled nerve growth factor (125I-NGF) revealed that approximately 35% of the cells bound NGF. The binding was specific and saturable; it was blocked by an excess of nonradioactive NGF, and was not detected following incubation with biologically inactive 125I-NGF. In addition, the binding did not appear to be blocked or diminished by insulin. Cell cultures prepared from somites or notochord showed no specific binding of 125I-NGF. Melanocytes comprised approximately 10% of the cell population in these cultures and appeared to be unlabeled. The subpopulation of cells with NGF receptors that were morphologically similar to other non-melanocyte unlabeled cells present in the neural crest cultures are probably the targets of the factor during differentiation and development. In contrast, there was no evidence of 125I-NGF binding by premigratory neural crest (adherent to the isolated neural tube) or by early migratory neural crest cells (24 hr after explantation). Both of these types of neural crest cells are relatively undifferentiated. The cells of the neural tube were also unlabeled. The binding of 125I-NGF to differentiating neural crest cells was not noticeably diminished by a brief pretreatment with trypsin or Dispase, enzymes used in the isolation of neural tubes. Hence, the absence of NGF receptors on premigratory neural crest and early migratory neural crest cultures was not due to enzymatic alterations of the receptor. It seems, therefore, that receptors for NGF appear on neural crest cells during the time when these cells are acquiring their phenotypic characteristics.

Animals↗
PubMed2003

Neural crest development is regulated by the transcription factor Sox9.

The neural crest is a transient migratory population of stem cells derived from the dorsal neural folds at the border between neural and non-neural ectoderm. Following induction, prospective neural crest cells are segregated within the neuroepithelium and then delaminate from the neural tube and migrate into the periphery, where they generate multiple differentiated cell types. The intrinsic determinants that direct this process are not well defined. Group E Sox genes (Sox8, Sox9 and Sox10) are expressed in the prospective neural crest and Sox9 expression precedes expression of premigratory neural crest markers. Here, we show that group E Sox genes act at two distinct steps in neural crest differentiation. Forced expression of Sox9 promotes neural-crest-like properties in neural tube progenitors at the expense of central nervous system neuronal differentiation. Subsequently, in migratory neural crest cells, SoxE gene expression biases cells towards glial cell and melanocyte fate, and away from neuronal lineages. Although SoxE genes are sufficient to initiate neural crest development they do not efficiently induce the delamination of ectopic neural crest cells from the neural tube consistent with the idea that this event is independently controlled. Together, these data identify a role for group E Sox genes in the initiation of neural crest development and later SoxE genes influence the differentiation pathway adopted by migrating neural crest cells.

Animals↗
PubMed2005

Embryology of the neural crest: its inductive role in the neurocutaneous syndromes.

Neural crest cells are first recognized at the lateral margin of the neural placode shortly after gastrulation, although they are not committed to their diverse fates until later. After dorsal closure of the neural tube, neural crest cells separate and migrate throughout the embryo to form many structures of ectodermal origin (eg, dorsal root and autonomic ganglia, peripheral nerve sheaths) and mesodermal origin (eg, blood vessels, melanocytes, adipose tissue, membranous bone, connective tissue, most of the ocular globe). Terminal differentiation occurs after migration is complete. Three regions of the neural tube generate neural crest: rhombencephalon, mesencephalon, and prosencephalon, each with a different migratory pattern. The most important genes promoting neural crest differentiation and migration are those with a dorsalizing influence in the vertical axis of the neural tube (eg, PAX3, BMP4, ZIC2), some segmentation genes (eg, WNT1), genes that inhibit neural crest (eg, EGR2), and neural crest-specific differentiating genes (eg, SLUG, SOX10). In the neurocutaneous syndromes, diverse features result from abnormal neural crest differentiation, providing a more encompassing embryologic basis for these disorders than the traditional view that these syndromes are somehow related to skin and brain because both are ectodermal derivatives. Abnormal angiogenesis, areas of abnormal pigmentation that sometimes follow the lines of Blashko, nerve sheath proliferations, disorders of chromaffin tissue, lipomes and benign and malignant tumors are frequent features. Many defective genes in neurocutaneous syndromes have an additional function as tumor suppressors. Interactions between genes associated with these disorders and others essential to neural crest formation, migration, and differentiation, are a likely molecular genetic basis for these diseases. The craniofacial abnormalities associated with many cerebral malformations and cutaneous lesions in some neurocutaneous syndromes emphasize an important inductive role of the neural tube in the development of non-neural tissues, mediated through neural crest.

Cell Differentiation↗
PubMed1993

Restriction of neurogenic ability during neural crest cell differentiation.

Multipotent neural crest cells undergo developmental restrictions during embryogenesis and eventually give rise to the neurons and glia of the peripheral nervous system, melanocytes, and pheochromocytes. To understand how neuronal potential is restricted to a subpopulation of crest-derived cells, we have utilized sensitive markers of early neuronal differentiation to assess neurogenesis in crest-derived cell populations subjected to defined experimental conditions in vitro and in vivo. We describe environmental conditions that either (a) result in the irreversible loss of neurogenic potential over a characteristic time course or (b) maintain neurogenic potential among neural crest cells.

Animals↗
PubMed2005

Central role of gene cooption in neural crest evolution.

A bona fide neural crest is a defining feature of vertebrate embryos. Protochordate gene expression patterns indicate that neural crest evolution coincided with the cooption of several transcriptional regulators to the neural plate border of the vertebrate ancestor. Recent cell labeling experiments in ascidians suggest that cells in this domain may have been migratory and thus displayed some neural crest cell-like behavior. Taken together, these data suggest that the recruitment of new genetic pathways conferred novel developmental potentials upon the migratory neural tube cells of the prevertebrate chordate.

Animals↗
PubMed1993

Regional differences between various axial segments of the avian neural crest regarding the formation of enteric ganglia.

The vagal neural crest adjacent to somites 1-7 gives rise to the enteric ganglia along the entire digestive tract. It is generally assumed that formation of enteric ganglia in preumbilical gut is independent of the axial segment from which the neural crest originates. In post-umbilical gut, however, there is evidence that the axial segment of origin of the neural crest might be relevant to neural differentiation. In this part of the gut, we previously identified a subpopulation of HNK-1-immunoreactive cells within the enteric mesenchyme. This immunoreactivity disappeared upon formation of the enteric nervous system. We studied the interaction between various axial segments of quail neural crest and the microenvironment in a neural chicken hindgut using chorioallantoic membrane cocultures. We found that neural crest cells from various axial segments could migrate into the gut and home to the correct sites. However, whereas vagal neural crest cells differentiated into enteric neurons, neural crest cells from truncal segments mainly differentiated into melanocytes. The HNK-1-immunoreactivity within the enteric mesenchyme only disappeared when neural crest cell colonization was followed by differentiation into enteric neurons and subsequent formation of enteric ganglia. To determine whether differentiation of neural crest cells in chorioallantoic membrane cocultures was influenced by the prolonged presence of the neural tube and notochord, we developed a new coculture system, using neural crest cells cultured in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗