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At least 19 recordsLinked to original sources
PubMed2024

A time-resolved single-cell roadmap of the logic driving anterior neural crest diversification from neural border to migration stages.

Neural crest cells exemplify cellular diversification from a multipotent progenitor population. However, the full sequence of early molecular choices orchestrating the emergence of neural crest heterogeneity from the embryonic ectoderm remains elusive. Gene-regulatory-networks (GRN) govern early development and cell specification toward definitive neural crest. Here, we combine ultradense single-cell transcriptomes with machine-learning and large-scale transcriptomic and epigenomic experimental validation of selected trajectories, to provide the general principles and highlight specific features of the GRN underlying neural crest fate diversification from induction to early migration stages using Xenopus frog embryos as a model. During gastrulation, a transient neural border zone state precedes the choice between neural crest and placodes which includes multiple converging gene programs. During neurulation, transcription factor connectome, and bifurcation analyses demonstrate the early emergence of neural crest fates at the neural plate stage, alongside an unbiased multipotent-like lineage persisting until epithelial-mesenchymal transition stage. We also decipher circuits driving cranial and vagal neural crest formation and provide a broadly applicable high-throughput validation strategy for investigating single-cell transcriptomes in vertebrate GRNs in development, evolution, and disease.

Animals↗
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.

Animals↗
PubMed1977

Independent expression of the adrenergic phenotype by neural crest cells in vitro.

Neural crest cells obtained from Japanese quail and grown in vitro without other embryonic tissues differentiate into adrenergic cells. These cells show intense catecholamine-specific histochemical fluorescence, and some have long, varicose neuronal processes. Ultrastructural examination shows two populations of cells, one with small (about 90 nm) dense-core vesicles resembling principal sympathetic neurons and the other with larger (about 150 nm) dense-core granules resembling chromaffin or small intensely fluorescent cells. Neuronal cells without adrenergic characteristics are also present. These results are compatible with the hypothesis that a population of cells determined along neuronal lines exists in the neural crest prior to migration.

Animals↗
PubMed1979

Ability of neural crest cells from the embryonic chick to differentiate into cartilage before their migration away from the neural tube.

Whether neural crest cells from the avian embryo are determined for chondrogenesis before they begin their migration away from the neural tube (i.e., before H. H. stages 8.5--9) was investigated by establishing neural folds from embryos of H. H. stages 5--11 either in organ culture, or as grafts to the chorioallantoic membranes of host embryos. Cartilage differentiated from neural folds taken from embryos of H. H. stages 5--7 but not from those taken from older embryos. This stage specific pattern was reversed when the tissue adjacent to the neural tube was grafted to the chorioallantoic membrane. Cartilage only formed from tissues isolated later than H. H. stage 8; i.e., when these adjacent tissues contain neural crest cells. We concluded that neural crest cells are determined for chondrogenesis while still in the neural tube and before their migration to the face and head. This is in contrast to the situation in the only other group which has been examined, the urodele amphibians.

Animals↗
PubMed1979

Electron microscope study on the contact of neural crest cells in the early stage of migration in bantam embryos.

The early stage of migration of neural crest cells was observed in the mid-brain level of bantam embryos (5-somite stage to 15-somite stage) by transmission) electron microscopy. It was confirmed that the migration of the neural crest cells starts at the stage of 7-8 somites and ends at the stage of about 14 somites. During this period, not only the contact of migrating crest cells with each other but also the contact between migrating cells and superficial ectodermal cells and/or neural tube cells was observed. Intercellular distance in those contact regions was 3-4 nm. The contact between the migrating crest cell and the basement membrane of the neural tube cell and of the ectodermal cell as well as the contact between the neural crest cell and the fibrillar structure in the environment was also seen. These findings suggest the possibility of transitory interaction for migration between neural crest cells with each other, between neural crest cells and cellular components of the environment where these crest cells migrate, and between neural crest cells and extracellular structures in the environment.

Animals↗
PubMed1979

Neural crest cells: temperature-dependent transformation by Rous sarcoma virus.

Cranial neural crest cells from chick embryos, when cultured under appropriate conditions, differentiate after approx. 1 week into pigmented cells. Neurol crest cells were infested with a mutant (RSV-BH-Ta) of the Bryan 'high titer' strain of Rous sarcoma virus on the second day of culture before the cells were morphologically differentiated, or later after they became pigmented. Cells infected and maintained at the temperature permissive for transformation (37 degrees C) proliferated rapidly compared to uninfected cells are produced extensive cytoplasmic vacuoles in a fashion similar to other types of cells transformed with RSV-BH-Ta at 37 degrees C. Cells infected and maintained at the non-permissive temperature for transformation (41 degrees C) also proliferated rapidly but did not become morphologically transformed. Transformation occurred reversibly following a shift of temperature. Infection of morphologically undifferentiated neural crest cells at either temperature prevented their differentiation into pigment cells, and infection of pigmented neural crest cells at either temperature led to a gradual loss of pigmentation. These results suggest that even at the non-permissive temperature the virus may regulate the state of differentiation of certain types of cells.

Animals↗
PubMed1977

Anionic glycopeptides and glycosaminoglycans synthesized by embryonic neural tube and neural crest.

Anionic glycopeptides and glycosaminoglycans synthesized by embryonic neural tube (epithelium) and neural crest (mesenchymal outgrowth) developing in vitro were examined. The profile of surface glycopeptides is relatively simple (two major ones for neural crest; four major ones for neural tube). There is one major glycopeptide found in the medium which is present only in trace amounts on the cells. Both hyaluronate and chondroitin sulfate are synthesized. Hyaluronate is predominantly cell associated; chondroitin sulfate is found predominantly in the medium. It is suggested that independent sorting of these relatively few glycopeptides can result in qualitative surface differences. Morphological state (epithelial or mesenchymal) and differentiated state may be related to these differences as well as to quantitative differences in surface glycosaminoglycans.

Animals↗
PubMed1978

Relationships between neural crest cells and catecholamine in suckling mice.

In suckling mice injected i.p. with a 27 mg/kg dose of L-hydrochloric acid isoproterenol, multiple neural crest tumors developed and cell death of neural crest cells occurred. It is speculated that neural crest derivatives may be beta-receptor cells and contain regulatory units of neurotransmission mediated through cyclic AMP.

Animals↗
PubMed2026

Defining active and repressive chromatin states in neural crest cells using low-input CUT&RUN.

The transition of neural crest cells (NCCs) from a multipotent state to lineage-restricted derivatives, including melanocytes, is governed by tightly regulated epigenetic mechanisms that orchestrate cell type specific gene expression programs. Histone post-translational modifications (PTMs), in particular, play an important role in modulating chromatin accessibility, enhancer activation, and transcription factor occupancy, thereby facilitating dynamic chromatin and transcriptional reprogramming required during development. However, profiling such chromatin states in rare and transient Neural Crest Cell (NCC) populations in vivo remains technically challenging. To address this, we present an optimized low-input Cleavage Under Targets and Release Using Nuclease (CUT&RUN) workflow tailored for fluorescence-activated cell sorting (FACS) isolated NCCs from zebrafish embryos. This approach enables high-resolution and low-background mapping of key histone modifications, including H3K27ac, H3K4me3, and H3K27me3, from limited cell numbers. Collectively, these methodologies provide a robust framework for dissecting chromatin state dynamics in developmental systems and can also offer insights into epigenetic dysregulation associated with disease.

Animals↗
PubMedDate not supplied

Acetylcholine synthesis by mesencephalic neural crest cells in the process of migration in vivo.

Specific to the vertebrate embryo, the neural crest is a transitory structure whose constituent cells migrate extensively through the developing animal and ultimately give rise to many distinct cell types, including the components of the peripheral nervous system. The earliest clear indices of their differentiation have so far been detected only when cells from the crest have reached their destination. This is exemplified by the acquisition of the ability to synthesise and store catecholamines; absent from crest cells before and during their dorso-ventral migration, this ability appears concomitantly with their aggregation into the primary sympathetic ganglia. The chronology of cholinergic maturation, however, is less well defined. Appropriate biochemical markers are demonstrable as soon as parasympathetic or enteric ganglia are formed, but the lack of a suitable cytochemical method is a major obstacle to the identification of any cholinergic cells before then. Although acetylcholinesterase (AChE) is present in migrating neural crest, choline acetyltransferase (CAT), the enzyme catalysing acetylcholine (ACh) synthesis, is a much more relevant correlate, and definitive evidence for cholinergic differentiation should include the demonstration of ACh-synthesising activity in intact cells or their extracts. We show here that neural crest, as soon as it begins migration, can synthesise ACh.

Acetylcholine↗
PubMed1976

An experimental investigation into the possible neural crest origin of pancreatic APUD (islet) cells.

It has recently been contended that pancreatic APUD cells are neural crest derivatives. In an experimental investigation, isotopic grafts of neural tube containing neural crest cells were transplanted from chick and quail embryos labelled with tritiated thymidine, and from unlabelled quail embryos, to host chick embryos at the same stage of development. Transplantations were performed at various levels between somites 5 and 24 in embryos at 6- to 24-somite stages. In operated embryos at 3 3/4 days of incubation, the pancreatic APUD cells were not labelled; nor did their nuclei show quail features. Migration of cells from the graft was evidenced by the presence of quail nuclei and/or radioactive label in autoradiographs, in spinal and sympathetic ganglia in the operated region. It is concluded that the pancreatic APUD cells of the 3 3/4-day-old chick embryo are not derived from the trunk neural crest up the level of somite 24. It is unlikely that more caudal levels contribute, because APUD cells are already concentrated in the dorsal pancreatic bud region at the 24-somite stage, by which time no migration of crest cells has occurred caudal to somite 24. This conclusion probably concerns A, B and D pancreatic endocrine cells.

Animals↗
PubMed1979

99mTc-methylene diphosphonate imaging in neural crest tumors.

Thirteen patients with neural crest tumors were each studied with a radionuclide skeletal survey, a radiographic skeletal survey, and an iliac crest bone marrow aspiration. The RN skeletal survey proved to be more accurate that the radiographic skeletal survey in: 1) detecting the primary tumor; 2) demonstrating bony metastatic disease; and 3) evaluating response to therapy. The overall accuracy of the RN skeletal survey in detecting metastatic disease correlated with the results of bone marrow aspiration both in the initial detection of metastatic disease and the evaluation of response during therapy.

Bone Neoplasms↗
PubMed1979

Morphology and behaviour of neural crest cells of chick embryo in vitro.

Neural primordia of chick embryos were cultured for three days and the behaviour of migrating neural crest cells studied. Somite cells were used as a comparison. Crest cells were actively multipolar with narrow projections which extended and retracted rapidly, contrasting to the gradual extension of somite-cell lamelleae. On losing cell contact, somite cells were also more directionally persistent. The rate of displacement of isolated crest cells was particularly low when calculated over a long time base. Both crest and somite cells were monolayered; contact paralysis occurred in somite cell collisions but was not ascertained for crest cells. However, crest cells in a population were far more directionally persistent than isolated cells. Contact duration between crest cells increased with time and they formed an open network. Eventually, retraction clumping occurred, initially and chiefly at the periphery of the crest outgrowth. Crest cells did not invade cultured embryonic mesenchymal or epithelial populations but endoderm underlapped them. No effects were observed on crest cells prior to direct contact. Substrate previously occupied by endoderm of ectoderm caused crest cells to flatten while substrate previously occupied by the neural tube caused them to round up and clump prematurely.

Animals↗
PubMed1977

Inhibition of cranial neural crest cell development by vitamin A in the cultured chick embryo.

Chick embryos at stage 8, prior to neural crest cell migration, were explanted on whole egg medium with or without vitamin A and cultured for 3 days. Sections through the head regions showed that the cranial neural crest cells had migrated into the first visceral arch in the controls but were absent from this structure in the treated embryos. These observations suggest that vitamin A inhibits neural crest cell development or migration, an effect which may in part account for the facial malformations produced by excess vitamin A.

Animals↗
PubMed1977

Development of choline acetyltransferase and cholinesterase activities in enteric ganglia derives from presumptive adrenergic and cholinergic levels of the neural crest.

The cholinergic differentiation of enteric ganglia in embryos of chick and quail was studied with particular reference to cholinesterase and choline acetyltransferase activities. Differentiation during normal development was compared with that obtained after culture of the neural primordium or neural crest in direct association with aneural hindgut. Biochemically differentiated cholinergic ganglia developed in explants containing cells from either the 'vagal' (presumptive cholinergic) or 'truncal' (presumptive adrenergic) levels of the neural crest. Neither extra-intestinal migration of neural crest cell nor the presence of central preganglionic fibres is a prerequisite for enteric ganglion differentiation.

Animals↗
PubMed1978

Harelip and cleft palate conditions in chick embryos following local destruction of the cephalic neural crest. A preliminary note.

With the aid of micro-laser irradiation, in a total of 156 chick embryos unilaterally (a part of) the cephalic neural crest paralleling the posterior portion of the prosencephalon and mesencephalon, was eliminated. As a result of this treatment, 2 out of 22 embryos, studied 24 hours after irradiation, showed a considerable degree of underdevelopment of the mesenchyme in the homolateral first branchial arch. At the age of 7 days (6 days after irradiation) 11 of the 44 surviving embryos proved to have developed a homolateral harelip condition. In 2 of these embryos, a wide palatal cleft was observed as well. These results demonstrate that facial clefts may develop as a result of a local deficiency of neural crest cells.

Animals↗