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PubMed1993

Protein growth factor requirements of rat neural crest cells.

Nascent neural crest cells derived from explanted E12 embryonic rat caudal neural tubes were used as an assay system to investigate the effects of fibroblast growth factors on neural crest cell (NCC) survival, proliferation, migration, and differentiation. In vitro and in vivo all NCC express low affinity nerve growth factor receptors (p75-LNGFR), whereas a subpopulation of NCC expresses the carbohydrate epitope recognized by the monoclonal antibody HNK-1 (Bannerman and Pleasure, manuscript in preparation). Both acidic and basic fibroblast growth factor (FGF) promoted the survival of proportionally greater numbers of p75-LNGF+/HNK-1- than P75-LNGFR+/HNK-1+ NCC. An as yet uncharacterized factor present in neural tube-conditioned medium was also required for NCC survival. Mitosis was frequent in those NCC closest to the neural tube, less so as the cells migrated away. Neither basic nor acidic fibroblast growth factor (FGF) influenced rates of NCC mitosis in either of these locations, nor did these FGFs alter the rate at which nascent NCC migrated away from the neural tube. However, acidic and basic FGFs did delay the differentiation of neural crest derived neurons in the cultures. FGF is abundant in the embryonic rat neural crest outgrowth zone, and the present study strongly supports an essential role for FGF in early development of the mammalian neural crest.

Animals↗
PubMed1993

Segregation of cell lineage in the neural crest.

Following neurulation, neural crest cells emerge from the neural tube and undergo extensive migrations. At the onset of migration, multipotent stem cells exist within the neural crest population. Eventually, these assume one of a number of possible fates, ranging from neurons and glia of the peripheral nervous system to pigment cells and cells of the facial skeleton. Neural crest cells follow migratory pathways and differentiate into derivatives that often are characteristic of their axial level of origin. Based on their stereotyped patterns of migration, limited intermixing and distinct homeobox-gene codes, some populations of neural crest cells may have a rostrocaudal regional identity imprinted prior to their emigration.

Animals↗
PubMed1997

Absence of neural crest cell regeneration from the postotic neural tube.

The preotic neural tube has a variable ability for regeneration of neural crest depending on the neuraxial level. There is robust regeneration of neural crest in the caudal midbrain/rostral hindbrain. In contrast, removal of the cardiac neural crest results in cardiovascular abnormalities suggesting the lack of regeneration in this area, although the regenerative capacity of the cardiac crest region has never been tested directly. Premigratory cardiac neural crest was ablated bilaterally using laser irradiation or extirpation by tungsten needle, and the remaining ventral neural tube was labeled with DiI to examine any neural crest regeneration from the neural tube. The results indicate that there is very little regeneration of crest cells from the cardiac region of the neural tube if the ablation is done prior to the 5-somite stage and no regeneration after the 6-somite stage with either ablation procedure. Furthermore no compensatory response occurs from the adjacent regions of the neural crest. By contrast, we were able to confirm that regeneration of neural crest occurs in the preotic rhombencephalic neural tube even after laser irradiation. An analysis in the trunk region suggests that the trunk neural tube is similar to the cardiac region in that it does not regenerate crest cells in the ventral migratory pathway after ablation. However, melanocytes generated cranial and caudal to the ablated region migrate radially and fill in the ablated region so that there is no interruption of the normal pigment pattern. This study indicates that even though there is a variable capacity for crest regeneration in the preotic neural tube, the postotic neural tube does not have such regenerative ability.

Animals↗
PubMed2002

Specification of zebrafish neural crest.

Analysis of neural crest cells in wild-type zebrafish and in isolated mutants has complemented studies in other organisms and has led to a greater understanding of the processes of cell fate and regional specification. Analysis of pigment cell development suggests that neural crest cell fate specification results from a combination of intrinsic cues such as differential expression of transcription factors and external factors such as the Wnts. Whether this model can be generalized to accommodate other neural crest cell fates remains an active area of research. Regional specification of neural crest appears to be coordinated by similar combinations of internal factors such as the hox genes, and extrinsic cues such as retinoic acid and endothelins. There is still a wealth of zebrafish mutations whose molecular bases remain unknown, and it is likely that the revelation of the underlying genes will both broaden and alter our understanding of specification within the neural crest.

Animals↗
PubMedDate not supplied

Monoclonal antibodies made to chick mesencephalic neural crest cells and to ciliary ganglion neurons identify a common antigen on the neurons and a neural crest subpopulation.

We previously reported the production of monoclonal antibodies (Mabs) that identified cell surface components of cultured chick and quail ciliary ganglion (CG) neurons and of a subpopulation of neural crest (NC) cells from 31-hr chick embryos (stage 9). Here we demonstrate that another Mab, CG-14, which was prepared to nitrocellulose-immobilized, lightly fixed (0.125% paraformaldehyde) mesencephalic NC cells from 31-hr (stage 9) chick embryos, labels the same antigen(s) recognized by CG-1 and CG-4 on both the CG neurons and the subpopulation of NC cells. All three Mabs label a polypeptide of 75 kD on Western blots of one-dimensional SDS-polyacrylamide gels. CG-14 blocked the binding of CG-1 and/or CG-4 to the 75 kD band on Western blots and blocked the binding of CG-1 and CG-4 to CG and NC cells. CG-1 and/or CG-4 antibodies, in turn, blocked the binding of CG-14 to Western blots, as well as NC and CG cells. We had previously shown that antibodies CG-1 and CG-4 were synergistically cytotoxic for the majority (95%) of cultured CG neurons in vitro in the presence of guinea pig complement. Here we show that the antibodies, which are both of the gamma 2a subclass, are also cytotoxic for the NC cells that they label in vitro. After the cells are ablated in culture, no other cells bearing the antigen(s) recognized by any of the three Mabs appear over a 2.5-week period. CG-14, however, is not cytotoxic for either the CG or NC cell populations alone or in combinations with CG-1 or CG-4. These results confirm our original observation that cultured CG neurons and NC cells share cell-surface antigen(s). The antigen recognized by all three Mabs appears to be the same whether the immunogen used to produce the antibodies was CG neurons or NC cells. This finding encourages us to continue tests of the hypothesis that the subpopulation of mesencephalic neural crest cells contributes to the formation of the ciliary ganglion in the embryo. Further characterization of the antigen appears in the accompanying paper.

Animals↗
PubMed1994

Genetic and epigenetic control in neural crest development.

The neural crest is a fascinating structure of the vertebrate embryo; its ontogeny includes a transient period during which its component cells undergo an epithelio-mesenchymal transition and become migratory. This phase was shown recently to be controlled by the 'Slug' gene which belongs to the 'Snail' family of Drosophila transcription factors. After homing to specific sites in the embryo, the crest-derived cells produce a large variety of phenotypes. Recent advances have shown that during migration most crest cells exhibit various degrees of pluripotentiality, some being already committed to a single and definite fate. Moreover, several lines of evidence point to the existence of totipotent stem cells in the neural crest, the progeny of which become progressively diversified through a combination of intrinsic and extrinsic influences. The latter have been documented by the disruption of several neurotrophin genes, which results in severe deficiencies of selected subsets of neural crest derivatives. The neural crest has also been shown to play an important role in the development of the vertebrate head and hypobranchial region. The genetic control of this process depends on the activity of developmental genes, among which the vertebrate Hox genes are essential, particularly at the rhombencephalic level.

Animals↗
PubMed2001

Induction and development of neural crest in Xenopus laevis.

Neural crest cells are a migratory embryonic cell population that form at the border between the neural plate and the future epidermis. This border, the neural plate border, corresponds to the neural fold. The neural fold surrounds the entire neural plate, but only the lateral and posterior portions of the fold give rise to neural crest cells, while the anterior neural fold differentiates as forebrain. This review focuses on neural crest development in Xenopus laevis embryos, and analyzes aspects of the induction of the neural crest in Xenopus, summarizing available information relating to the expression of several genes in the neural crest. Two models for neural crest induction are discussed. In the first model, the neural crest is induced by the interaction between the neural plate and the epidermis. In the second, the specification of the neural plate border arises as a consequence of a gradient of BMP activity. The role of posteriorizing signals on neural crest specification is also discussed. Finally, we propose that the specification and differentiation of the neural crest is controlled by a cascade of transcription factors, encoded and expressed from a hierarchy of genes. A set of extracellular signals establishes the positional information in the ectoderm, which activates Prepattern genes (Gli, Xiro, Zic, Dlx, etc.) across extended and overlapping domains. A local combination of these genes at the neural plate border activates the cascade of neural crest specification, while different sets of genes are activated at both sides of the neural folds (in the epidermis and the neural plate). The genes activated in regions adjacent to the neural plate border have an inhibitory effect on the neural crest transcription program.

Animals↗
PubMed1992

Effect of insulin and insulin-like growth factor I on the expression of the catecholaminergic phenotype by neural crest cells.

Neural crest-derived catecholaminergic precursors have been used as a model to study the role of signals supplied by the environment during avian neurogenesis. A new culture system consisting of dissociated sclerotomes or somites isolated at embryonic day 3 (E3) or 2.5 (E2.5) has been established, which allows quantitative comparison of various culture conditions. As a first step of this study, the role of insulin and insulin-like growth factor I (IGF-I) in catecholaminergic differentiation has been investigated. Our results show that both factors are able to increase by a factor 2 to 3 the number of catecholaminergic cells present in the culture of sclerotomes after 24 h of culture. The effect is dose-dependent and the half-maximal effect is obtained with low concentrations of each peptide. Since insulin, IGF-I and their respective receptors are present at this stage of development in avian embryo, our observations suggest that an early step in catecholaminergic differentiation could be under at least the partial control of insulin and insulin-related peptides. On the other hand, neural crest precursors isolated at E2.5 are not able to generate catecholaminergic cells and to respond to insulin when cultivated for one day, indicating that these precursors are subjected in vivo to a maturation step, within the somite/sclerotome between E2.5 and E3; this step could be obtained in vitro by cultivating the precursors for 1 day, which resulted in the development of insulin responsiveness by catecholaminergic precursors.

Animals↗
PubMed1996

Regulative interactions in zebrafish neural crest.

Zebrafish trunk neural crest cells that migrate at different times have different fates: early-migrating crest cells produce dorsal root ganglion neurons as well as glia and pigment cells, while late-migrating crest cells produce only non-neuronal derivatives. When presumptive early-migrating crest cells were individually transplanted into hosts such that they migrated late, they retained the ability to generate neurons. In contrast, late-migrating crest cells transplanted under the same conditions never generated neurons. These results suggest that, prior to migration, neural crest cells have intrinsic biases in the types of derivatives they will produce. Transplantation of presumptive early-migrating crest cells does not result in production of dorsal root ganglion neurons under all conditions suggesting that these cells require appropriate environmental factors to express these intrinsic biases. When early-migrating crest cells are ablated, late-migrating crest cells gain the ability to produce neurons, even when they migrate on their normal schedule. Interactions among neural crest cells may thus regulate the types of derivatives neural crest cells produce, by establishing or maintaining intrinsic differences between individual cells.

Animals↗
PubMed2005

Early steps in neural crest specification.

The neural crest is a multipotent cell population that arise at the border of the neural plate and non-neural ectoderm. Studies conducted in a number of model organisms including chickens, frogs, zebrafish and mice have been instrumental in elucidating this molecular mechanisms underlying neural crest formation. Signaling molecules of the Wnt, BMP, and FGF families and their downstream effectors have been shown to mediate neural crest induction. Transcription factors including members of the Snail and SoxE gene families as well as FoxD3, c-Myc and others have been implicated in specification of the neural crest. These studies represent an important step in understanding the regulatory interactions involved in generating this complex and interesting cell type.

Animals↗
PubMed1997

Analysis of neural crest cell migration in Splotch mice using a neural crest-specific LacZ reporter.

Studies on the mouse Splotch (Sp) mutation, a deletion in the transcription factor Pax-3, have revealed that Pax-3 is essential for normal development of the neural crest. We have investigated the defect in neural crest development using a Wnt-l::LacZ reporter construct to mark neural crest cells. Staining embryos for beta-galactosidase activity at different developmental stages revealed a severe reduction in the number of neural crest cells which emigrated from the neural tube at the vagal and rostral trunk levels. At the caudal thoracic, lumbar, and sacral levels there was a complete loss of neural crest cell emigration. In contrast to previous work in culture, we saw no evidence for any delay in the onset of neural crest cell migration at anterior levels. Pax-3 is expressed in the dorsal neural tube, where the neural crest cells originate, in migrating neural crest cells, and in somitic cells along the migratory pathway. Hence, it is not clear which aspect of the Pax-3 expression accounts for the observed phenotype. We addressed this problem by transplanting neural tissue between mouse and chick embryos. Our studies indicate that the defect in the Splotch mutation is not intrinsic to the neural crest cells themselves, but appears to reflect inappropriate cell interactions either within the neural tube or between the neural tube and the somite.

Animals↗
PubMed1988

Nodose placode provides ectomesenchyme to the developing chick heart in the absence of cardiac neural crest.

The cardiac neural crest provides both ectomesenchyme and parasympathetic postganglionic neurons to the developing heart. Ablation of cardiac neural crest results in persistent truncus arteriosus, a condition in which the conotruncal and aorticopulmonary septa do not form in the developing heart. Parasympathetic postganglionic neurons are abundantly present in hearts with persistent truncus arteriosus, which indicates a "regeneration" of the neural component of the cardiac neural crest without comparable restitution of the ectomesenchymal component. The neural component has been shown to be provided by cells from the nodose placode following ablation of the cardiac neural crest. This investigation has shown that ectomesenchymal cells are also supplied to a limited extent by the nodose placode which normally has no ectomesenchymal derivatives. Although placode-derived ectomesenchyme helps to strengthen the wall of the cardiac outflow vessel, it is not competent to induce conotruncal and aorticopulmonary septal closure.

Animals↗
PubMed1984

On the differentiation and migration of some non-neuronal neural crest derived cell types.

Neural tubes containing premigratory neural crest cells from head and trunk levels as well as somites containing neural crest cells that have migrated away from the neural crest were grafted orthotopically and heterotopically from quail embryos to chicken embryos. Schwann cells and melanocytes of donor origin developed after all grafting procedures. Cartilage developed only from neural crest cells of head levels. No skeletal muscle was ever observed to develop from the neural crest. The development of these different cell types from heterotopically grafted premigratory neural crest cells indicates that the neural crest is not a population of pluripotent undeterminated cells, but that at least some determinated cells are present within it before the onset of emigration of neural crest cells from the neural crest. Different neural-crest-derived cell populations exhibit different migratory behaviour: After heterotopically grafting quail neural crest cells to the wing buds of chicken embryos, Schwann cells and non-epidermal melanocytes were found to have migrated proximally and distally away from the grafts. Epidermal melanocytes of donor origin were found to have migrated in a distal direction essentially.

Animals↗
PubMed2006

Model systems for the study of heart development and disease. Cardiac neural crest and conotruncal malformations.

Neural crest cells are multipotential cells that delaminate from the dorsal neural tube and migrate widely throughout the body. A subregion of the cranial neural crest originating between the otocyst and somite 3 has been called "cardiac neural crest" because of the importance of these cells in heart development. Much of what we know about the contribution and function of the cardiac neural crest in cardiovascular development has been learned in the chick embryo using quail-chick chimeras to study neural crest migration and derivatives as well as using ablation of premigratory neural crest cells to study their function. These studies show that cardiac neural crest cells are absolutely required to form the aorticopulmonary septum dividing the cardiac arterial pole into systemic and pulmonary circulations. They support the normal development and patterning of derivatives of the caudal pharyngeal arches and pouches, including the great arteries and the thymus, thyroid and parathyroids. Recently, cardiac neural crest cells have been shown to modulate signaling in the pharynx during the lengthening of the outflow tract by the secondary heart field. Most of the genes associated with cardiac neural crest function have been identified using mouse models. These studies show that the neural crest cells may not be the direct cause of abnormal cardiovascular development but they are a major component in the complex tissue interactions in the caudal pharynx and outflow tract. Since, cardiac neural crest cells span from the caudal pharynx into the outflow tract, they are especially susceptible to any perturbation in or by other cells in these regions. Thus, understanding congenital cardiac outflow malformations in human sequences of malformations as represented by the DiGeorge syndrome will necessarily require understanding development of the cardiac neural crest.

Animals↗
PubMed2001

FGF-8 in the ventral pharynx alters development of myocardial calcium transients after neural crest ablation.

Cardiac neural crest ablation results in depressed myocardial calcium transients and elevated proliferation in myocardium at a stage when cardiac neural crest cells are not in contact with the myocardium. To test the hypothesis that cardiac neural crest-derived cells, which migrate into the caudal, ventral pharynx at stage 14, block a signal from the ventral pharynx, we cultured stage 12 chick heart tube or myocardial strips in the presence or absence of ventral pharynx. We found that myocardium cultured with ventral pharynx that had not yet contacted neural crest cells had significantly reduced calcium transients and an increased rate of proliferation. Ventral pharynx from intact embryos at a stage when neural crest-derived cells had reached the pharynx had no effect on myocardial calcium transients. Ventral pharynx from neural crest-ablated embryos continued to suppress myocardial calcium transients at this later stage. Myocardium cultured with FGF-2 also showed a significant reduction in calcium transients. An FGF-2-neutralizing Ab reversed the deleterious effect of the ventral pharynx on myocardial calcium transients and proliferation. We therefore examined the expression of FGF-2 and similar FGFs in the ventral pharynx. Only FGF-8 was expressed in a temporospatial pattern that made it a viable candidate for altering the myocardial calcium transient during stages 14-18. In explant cultures, neutralizing Ab for FGF-8 rescued development of the myocardial calcium transient in neural crest-ablated chick embryos.

Animals↗
PubMed2005

Essential role of non-canonical Wnt signalling in neural crest migration.

Migration of neural crest cells is an elaborate process that requires the delamination of cells from an epithelium and cell movement into an extracellular matrix. In this work, it is shown for the first time that the non-canonical Wnt signalling [planar cell polarity (PCP) or Wnt-Ca2+] pathway controls migration of neural crest cells. By using specific Dsh mutants, we show that the canonical Wnt signalling pathway is needed for neural crest induction, while the non-canonical Wnt pathway is required for neural crest migration. Grafts of neural crest tissue expressing non-canonical Dsh mutants, as well as neural crest cultured in vitro, indicate that the PCP pathway works in a cell-autonomous manner to control neural crest migration. Expression analysis of non-canonical Wnt ligands and their putative receptors show that Wnt11 is expressed in tissue adjacent to neural crest cells expressing the Wnt receptor Frizzled7 (Fz7). Furthermore, loss- and gain-of-function experiments reveal that Wnt11 plays an essential role in neural crest migration. Inhibition of neural crest migration by blocking Wnt11 activity can be rescued by intracellular activation of the non-canonical Wnt pathway. When Wnt11 is expressed opposite its normal site of expression, neural crest migration is blocked. Finally, time-lapse analysis of cell movement and cell protrusion in neural crest cultured in vitro shows that the PCP or Wnt-Ca2+ pathway directs the formation of lamellipodia and filopodia in the neural crest cells that are required for their delamination and/or migration.

Adaptor Proteins, Signal Transducing↗
PubMed2004

Cardiac outflow tract defects in mice lacking ALK2 in neural crest cells.

Cardiac neural crest cells are multipotent migratory cells that contribute to the formation of the cardiac outflow tract and pharyngeal arch arteries. Neural crest-related developmental defects account for a large proportion of congenital heart disorders. Recently, the genetic bases for some of these disorders have been elucidated, and signaling pathways required for induction, migration and differentiation of cardiac neural crest have emerged. Bone morphogenetic proteins comprise a family of secreted ligands implicated in numerous aspects of organogenesis, including heart and neural crest development. However, it has remained generally unclear whether BMP ligands act directly on neural crest or cardiac myocytes during cardiac morphogenesis, or function indirectly by activating other cell types. Studies on BMP receptor signaling during organogenesis have been hampered by the fact that receptor knockouts often lead to early embryonic lethality. We have used a Cre/loxP system for neural crest-specific deletion of the type I receptor, ALK2, in mouse embryos. Mutant mice display cardiovascular defects, including persistent truncus arteriosus, and abnormal maturation of the aortic arch reminiscent of common forms of human congenital heart disease. Migration of mutant neural crest cells to the outflow tract is impaired, and differentiation to smooth muscle around aortic arch arteries is deficient. Moreover, in Alk2 mutants, the distal outflow tract fails to express Msx1, one of the major effectors of BMP signaling. Thus, the type I BMP receptor ALK2 plays an essential cell-autonomous role in the development of the cardiac outflow tract and aortic arch derivatives.

Activin Receptors, Type I↗
PubMed2006

Cooperative action of Sox9, Snail2 and PKA signaling in early neural crest development.

In neural crest formation, transcription factors, such as group E Sox and Snail1/Snail2 (Slug) regulate subsequent epithelial-mesenchymal transition (EMT) and migration. In particular, Sox9 has a strong effect on neural crest formation, EMT and differentiation of crest-derived cartilages in the cranium. It remains unclear, however, how Sox9 functions in these events, and how Sox9 activity is regulated. In this study, our gain-of-function and loss-of-function experiments reveal that Sox9 is essential for BMP signal-mediated induction of Snail2 and subsequent EMT in avian neural crest. We also show that Snail2 activates the Snail2 promoter, although Snail family proteins have been known as a repressor. Consistently, Sox9 directly activates the Snail2 promoter in synergy with, and through a direct binding to, Snail2. Finally, functions of these transcription factors in neural crest cells are enhanced by PKA signaling.

Animals↗