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PubMed2006

In vivo analysis reveals a critical role for neuropilin-1 in cranial neural crest cell migration in chick.

The neural crest provides an excellent model system to study invasive cell migration, however it is still unclear how molecular mechanisms direct cells to precise targets in a programmed manner. We investigate the role of a potential guidance factor, neuropilin-1, and use functional knockdown assays, tissue transplantation and in vivo confocal time-lapse imaging to analyze changes in chick cranial neural crest cell migratory patterns. When neuropilin-1 function is knocked down in ovo, neural crest cells fail to fully invade the branchial arches, especially the 2nd branchial arch. Time-lapse imaging shows that neuropilin-1 siRNA transfected neural crest cells stop and collapse filopodia at the 2nd branchial arch entrances, but do not die. This phenotype is cell autonomous. To test the influence of population pressure and local environmental cues in driving neural crest cells to the branchial arches, we isochronically transplanted small subpopulations of DiI-labeled neural crest cells into host embryos ablated of neighboring, premigratory neural crest cells. Time-lapse confocal analysis reveals that the transplanted cells migrate in narrow, directed streams. Interestingly, with the reduction of neuropilin-1 function, neural crest cells still form segmental migratory streams, suggesting that initial neural crest cell migration and invasion of the branchial arches are separable processes.

Animals↗
PubMed1993

Plasticity in neural crest cell differentiation.

The neural crest is a pluripotent population of cells that are endowed with migratory capacities. It has long been known that the differentiation pathway taken by cells derived from the neural crest is largely controlled by the microenvironment to which they home after their migration phase, indicating a high degree of plasticity in their developmental fate. Recent progress has been made concerning the factors which influence survival, growth and differentiation of selected sets of precursors in each embryonic site colonised by derivatives of the neural crest.

Adrenal Medulla↗
PubMed1985

Changes in cholinergic parameters associated with failure of conotruncal septation in embryonic chick hearts after neural crest ablation.

Cells from the neural crest over occipital somites migrate to the heart, where they give rise to parasympathetic postganglionic neurons as well as ectomesenchymal elements which contribute to conotruncal septation. With a microcautery needle, the neural crest over occipital somites was ablated bilaterally in chicken embryos at an early stage of development. Histological examination on incubation day 15 revealed conotruncal malformations, involving malformation or absence of the conotruncal septum in all embryos. Two peaks of embryo mortality were observed. One peak (incubation days 6-8) occurred at the same time as conotruncal septal closure; the second peak (incubation days 11-13) was concurrent with the onset of functional parasympathetic innervation. A disruption of parasympathetic innervation was indicated by: (1) a decrease in acetylcholinesterase staining, (2) a decrease (27%) in the number of ganglion cells in the conotruncus, (3) decreases in the acetylcholine content of atrium (31%) and ventricle (39%), and (4) a decrease (21%) in muscarinic acetylcholine receptor density on incubation day 15. Radiolabeled ligand-binding studies revealed no change in the affinity of cardiac muscarinic receptors for [3H]methylscopolamine (KD = 0.17-0.21 nM). Agonist-binding affinity and sensitivity to guanine nucleotides were similarly unaffected. The reasons for the limited extent of the parasympathetic lesion are unclear, but may involve recruitment of precursor cells from other regions of the neural crest, partial regeneration of the neural crest following surgical removal, or an alteration in the contribution of incoming sympathetic or preganglionic parasympathetic elements. No such plasticity was associated with neural crest contributions to the structural development of the conotruncus. Malformations were observed in all lesioned embryos.

Acetylcholine↗
PubMed1994

Ciliary neurotrophic factor (CNTF) has a dose-dependent biphasic effect on the number of adrenergic cells which develop in avian trunk neural crest cultures.

The embryonic neural crest is the source of progenitor cells for a wide variety of adult cell types including several populations of neurons and neuroendocrine cells. We have investigated the effect of ciliary neurotrophic factor (CNTF) on the development of quail trunk neural crest cultures. We found that at low doses CNTF promoted the development of increased numbers of adrenergic cells, but higher doses resulted in a decreased number of adrenergic cells relative to controls. Total and melanocyte cell number were unaffected over the range of CNTF concentrations tested. These results indicate that CNTF can affect adrenergic development in neural crest cultures in a dose-dependent biphasic manner.

Animals↗
PubMed1990

The microenvironment created by grafting rostral half-somites is mitogenic for neural crest cells.

Chicken embryo neural crest cells that migrate into a paraxial mesoderm constructed of multiple rostral half-somites from quail embryos form unsegmented "polyganglia," instead of distinct dorsal root ganglia (DRG). We report here that the environment that is created by grafting rostral somitic (RS) moieties not only is permissive for neural crest cell migration and consequent DRG formation but also is mitogenic for the DRG precursor cells. On embryonic day 3.5 (E3.5), 1 day after surgery, there is a 42% average increase in volume of the polyganglia compared with the corresponding DRG on the unoperated side. The volume increase is accounted for by an increased number of DRG cells--an average of 46% more cells are found in the polyganglia. The increases in volume and cell number are still present a day later at E4.5 (38% and 52%, respectively) and are observed in both limb-forming and non-limb-forming regions of the embryonic axis. The mechanism for this increase in cell number and volume in the polyganglia is enhanced proliferative activity. On E3.5 the proportion of cells incorporating thymidine of the total DRG cell number is 45% higher in the polyganglia than the control side, when embryos are given a short pulse before sacrifice. This indicates that rostral sclerotomal environment stimulates the crest cells to proliferate. The difference in volume between the polyganglia and the normal DRG continues to grow until at least E8, when the polyganglia are twice as large as the control DRG. The continued increase in volume can also be accounted for by the mitogenic effect of the RS grafts, since on E4.5 the percentage of thymidine-labeled cells compared with the total cell number in DRG is 28% higher in the polyganglia than in control ganglia. This study demonstrates that the somitic microenvironment regulates the proliferation of neural crest cells in the nascent DRG.

Animals↗
PubMed2005

Role of morphogens in neural crest cell determination.

The neural crest is a transient, migratory cell population found in all vertebrate embryos that generate a diverse range of cell and tissue derivatives including, but not limited, to the neurons and glia of the peripheral nervous system, smooth muscle, connective tissue, melanocytes, craniofacial cartilage, and bone. Over the past few years, many studies have provided tremendous insights into understanding the mechanisms regulating the induction and migration of neural crest cell development. This review highlights the surprising and perhaps unexpected roles for morphogens in these distinct processes. A comparison of studies performed in several different vertebrates emphasizes the requirement for coordination between multiple signaling pathways in the induction and migration of neural crest cells in the developing embryo.

Amphibians↗
PubMed2006

Neural crest stem and progenitor cells.

Neural crest cells are a multipotent, migratory cell population that generates an astonishingly diverse array of cell types during vertebrate development. These include bones; tendons; neurons; glia; melanocytes; and connective, endocrine, and adipose tissue. With a limited capacity for self-renewal and a wide range of differentiation fates, neural crest cells bear many of the hallmarks of stem cells and persist throughout embryonic and adult development. But are all neural crest cells true stem cells, or do the majority of neural crest cells more closely resemble progenitor cells? In this review we discuss recent advances in characterizing the properties of neural crest cells, together with their potential for tissue-specific repair.

Animals↗
PubMed2002

Bimodal functions of Notch-mediated signaling are involved in neural crest formation during avian ectoderm development.

Neural crest is induced at the junction of epidermal ectoderm and neural plate by the mutual interaction of these tissues. In previous studies, BMP4 has been shown to pattern the ectodermal tissues, and BMP4 can induce neural crest cells from the neural plate. In this study, we show that epidermally expressed Delta1, which encodes a Notch ligand, is required for the activation and/or maintenance of Bmp4 expression in this tissue, and is thus indirectly required for neural crest induction by BMP4 at the epidermis-neural plate boundary. Notch activation in the epidermis additionally inhibits neural crest formation in this tissue, so that neural crest generation by BMP4 is restricted to the junction.

Animals↗
PubMed2005

The transcriptional control of trunk neural crest induction, survival, and delamination.

Trunk neural crest cells are generated at the border between the neural plate and nonneural ectoderm, where they initiate a distinct program of gene expression, undergo an epithelial-mesenchymal transition (EMT), and delaminate from the neuroepithelium. Here, we provide evidence that members of three families of transcription induce these properties in premigratory neural crest cells. Sox9 acts to provide the competence for neural crest cells to undergo an EMT and is required for trunk neural crest survival. In the absence of Sox9, cells apoptose prior to or shortly after delamination. Slug/Snail, in the presence of Sox9, is sufficient to induce an EMT in neural epithelial cells, while FoxD3 regulates the expression of cell-cell adhesion molecules required for neural crest migration. Together, the data suggest a model in which a combination of transcription factors regulates the acquisition of the diverse properties of neural crest cells.

Animals↗
PubMed1983

The use of chlorotetracycline to localize calcium in neural crest cells.

Cultured amphibian neural crest cells in the early phases of migration (1-2 days) extend broad, clear cytoplasmic processes known as lobopodia. These regions exhibit rapid changes in the contraction-relaxation cycle and in substratum adhesion. Because of the putative role of Ca2+ in both cytoskeletal function and cell attachment, its distribution in these cells was studied. Chlorotetracycline (CTC), the Ca2+-chelating fluorescent probe, was used to investigate whether there is a temporal and spatial localization of Ca2+ in cell regions concerned with movement and attachment. Differentiated neural crest cells (7 days), which contain an abundance of actin stress fibers, were also studied to determine whether these cytoskeletal elements were associated with Ca2+. The results with CTC indicate that in early migratory cells regions of membrane extension and protrusion contain higher levels of Ca2+ and that the actin stress fiber system of differentiating neural crest cells (7 days) is associated with Ca2+. It was determined that using the CTC in the fixative produced the same labeling profile as when live cells were labeled with the CTC. Use of CTC in the fixative is a decided advantage over treatment of cells with CTC while alive since it avoids the photooxidative damage which normally accompanies fluorescent observations of CTC on living cells.

Actins↗
PubMed1992

Statistical evidence for a random commitment of pluripotent cephalic neural crest cells.

The neural crest (NC) of vertebrate embryos yields cell types belonging to the neural, melanocytic and mesectodermal lineages. To test the possibility that the precursors of these lineages segregate from pluripotent cells by a process involving stochastic determinants, we have analyzed with statistical methods the associations between six differentiated cell types in 201 clones obtained in vitro from migrating cephalic NC cells. Our analysis suggests that neuronal, adrenergic and Schwann cells are not randomly associated, whereas these neural cell types differentiate in the clones independently of both melanocytes and cartilage. These results raise the possibility that pluripotent NC progenitors give rise to the precursors of the major NC-derived lineages (neural, melanocytic and mesectodermal) by a process involving stochastic restrictions of their developmental potentialities.

Animals↗
PubMed1992

Isolation of a stem cell for neurons and glia from the mammalian neural crest.

We have isolated mammalian neural crest cells using a monoclonal antibody to the low affinity NGF receptor, and established conditions for the serial propagation of these cells in clonal culture to assess their developmental potential. This analysis indicates that, first, single mammalian neural crest cells are multipotent, able to generate at least neurons and Schwann cells like their avian counterparts. Second, multipotent neural crest cells generate multipotent progeny, indicating that they are capable of self-renewal and therefore are stem cells. Third, multipotent neural crest cells also generate some clonal progeny that form only neurons or glia, suggesting the production of committed neuroblasts and glioblasts. Manipulation of the substrate alters the fate of the multipotent cells. These findings have implications for models of neural crest development in vivo, and establish a system for studying the generation of cellular diversity by a multipotent stem cell in vitro.

Animals↗
PubMed2005

Neural crest migration methods in the chicken embryo.

Neural crest cells emerge from the neural tube early in development. They migrate extensively throughout the embryo and form most of the head and peripheral nervous system, giving rise to sensory and sympathetic ganglia, heart regions, adrenal cells, head bones, teeth, muscle cells, sensory organs, melanocytes, and other cell types. The neural crest is interesting because of its unique origin, development and differentiation. These cells are initially part of the dorsal neural tube, with a clear epithelial character; later, they transform into actively motile mesenchymal cells. Little is known about the underlying mechanism directing this process. It remains unknown why neural crest cells target particular derivatives (neurons, heart muscle and glia) and body regions (peripheral nerves, heart, skin, head and gut). Neural crest migration can be divided into three stages: 1) emigration from the neural tube; 2) migration along defined pathways; and 3) cessation of migration. At the onset of migration, neural crest cells lose their epithelial nature within the neural tube and transform into a migratory, mesenchymal cell type. Neural crest development has been best studied in avian embryos, which are amenable to surgical manipulation, cell marking techniques, cell culture and transgenesis by electroporation and retrovirally mediate gene transfer. The methods outlined below are those typically used to study and understand the different factors and signals necessary for the neural crest development before and during their migration.

Animals↗
PubMed1999

A novel transgenic technique that allows specific marking of the neural crest cell lineage in mice.

Neural crest cells are embryonic, multipotent stem cells that give rise to various cell/tissue types and thus serve as a good model system for the study of cell specification and mechanisms of cell differentiation. For analysis of neural crest cell lineage, an efficient method has been devised for manipulating the mouse genome through the Cre-loxP system. We generated transgenic mice harboring a Cre gene driven by a promoter of protein 0 (P0). To detect the Cre-mediated DNA recombination, we crossed P0-Cre transgenic mice with CAG-CAT-Z indicator transgenic mice. The CAG-CAT-Z Tg line carries a lacZ gene downstream of a chicken beta-actin promoter and a "stuffer" fragment flanked by two loxP sequences, so that lacZ is expressed only when the stuffer is removed by the action of Cre recombinase. In three different P0-Cre lines crossed with CAG-CAT-Z Tg, embryos carrying both transgenes showed lacZ expression in tissues derived from neural crest cells, such as spinal dorsal root ganglia, sympathetic nervous system, enteric nervous system, and ventral craniofacial mesenchyme at stages later than 9.0 dpc. These findings give some insights into neural crest cell differentiation in mammals. We believe that P0-Cre transgenic mice will facilitate many interesting experiments, including lineage analysis, purification, and genetic manipulation of the mammalian neural crest cells.

Animals↗
PubMed2006

Development of the neural crest: achieving specificity in regulatory pathways.

Recent studies have revealed the signaling pathways and downstream effectors involved in the specification of the neural crest. Neural crest cells are generated from a zone at the neurectoderm border in response to Wnt and BMP signals. BMP signals are involved in establishing a competency zone at the border of the neurectoderm, while subsequent Wnt signals specify neural crest cells. Combinations of transcription factors, including pax and msx gene products, act downstream of these pathways to integrate signals and establish the neural crest. Mechanisms are emerging for how specificity is generated from reiterated signals and effectors.

Animals↗
PubMed2002

Amphioxus and lamprey AP-2 genes: implications for neural crest evolution and migration patterns.

The neural crest is a uniquely vertebrate cell type present in the most basal vertebrates, but not in cephalochordates. We have studied differences in regulation of the neural crest marker AP-2 across two evolutionary transitions: invertebrate to vertebrate, and agnathan to gnathostome. Isolation and comparison of amphioxus, lamprey and axolotl AP-2 reveals its extensive expansion in the vertebrate dorsal neural tube and pharyngeal arches, implying co-option of AP-2 genes by neural crest cells early in vertebrate evolution. Expression in non-neural ectoderm is a conserved feature in amphioxus and vertebrates, suggesting an ancient role for AP-2 genes in this tissue. There is also common expression in subsets of ventrolateral neurons in the anterior neural tube, consistent with a primitive role in brain development. Comparison of AP-2 expression in axolotl and lamprey suggests an elaboration of cranial neural crest patterning in gnathostomes. However, migration of AP-2-expressing neural crest cells medial to the pharyngeal arch mesoderm appears to be a primitive feature retained in all vertebrates. Because AP-2 has essential roles in cranial neural crest differentiation and proliferation, the co-option of AP-2 by neural crest cells in the vertebrate lineage was a potentially crucial event in vertebrate evolution.

Ambystoma↗
PubMed2003

Dissimilar regulation of cell differentiation in mesencephalic (cranial) and sacral (trunk) neural crest cells in vitro.

During development neural crest cells give rise to a wide variety of specialized cell types in response to cytokines from surrounding tissues. Depending on the cranial-caudal level of their origin, different populations of neural crest cells exhibit differential competence to respond to these signals as exemplified by the unique ability of cranial neural crest to form skeletal cell types. We show that in addition to differences in whether they respond to particular signals, cranial neural crest cells differ dramatically from the trunk neural crest cells in how they respond to specific extracellular signals, such that under identical conditions the same signal induces dissimilar cell fate decisions in the two populations in vitro. Conversely, the same differentiated cell types are induced by different signals in the two populations. These in vitro differences in neural crest response are consistent with in vivo manipulations. We also provide evidence that these differences in responsiveness are modulated, at least in part, by differential expression of Hox genes within the neural crest.

Animals↗
PubMed1997

Isolation and characterization of chondroitin sulfate proteoglycans from embryonic quail that influence neural crest cell behavior.

The movement of neural crest cells is controlled in part by extracellular matrix. Aggrecan, the chondroitin sulfate proteoglycan from adult cartilage, curtails the ability of neural crest cells to adhere, spread, and move across otherwise favorable matrix substrates in vitro. Our aim was to isolate, characterize, and compare the structure and effect on neural crest cells of aggrecan and proteoglycans purified from the tissues through which neural crest cells migrate. We metabolically radiolabeled proteoglycans in E2.5 quail embryos and isolated and characterized proteoglycans from E3.3 quail trunk and limb bud. The major labeled proteoglycan was highly negatively charged, similar in hydrodynamic size to chick limb bud versican/PG-M, smaller than adult cartilage aggrecan but larger than reported for embryonic sternal cartilage aggrecan. The molecular weight of the iodinated core protein was about 400 kDa, which is more than reported for aggrecan but less than that of chick versican/PG-M. The proteoglycan bore chondroitin sulfate glycosaminoglycan chains of 45 kDa, which is larger than those of aggrecan. It lacked dermatan sulfate, heparan sulfate, or keratan sulfate chains. It bound to collagen type I, like aggrecan, but not to fibronectin (unlike versican/PG-M), collagen type IV, or laminin-1 in solid-phase assays and it bound to hyaluronate in gel-shift assays. When added at concentrations between 10 and 30 microg/ml to substrates of fibronectin, trunk proteoglycan inhibited neural crest cell spreading and migration. Attenuation of cell spreading was shown to be the most sensitive and titratable measure of the effect on neural crest cells. This effect was sensitive to digestion with chondroitinase ABC. Similar cell behavior was also produced by aggrecan and the small dermatan sulfate proteoglycan decorin; however, 30-fold more aggrecan was required to produce an effect of similar magnitude. When added in solution to neural crest cells which were already spread and migrating on fibronectin, the embryonic proteoglycan rapidly and reversibly caused complete rounding of the cells, being at least 30-fold more potent than aggrecan in this activity.

Aggrecans↗