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Journal articles on the topic 'Neural crest cells'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Bronner-Fraser, Marianne, and Scott E. Fraser. "Cell lineage analysis of the avian neural crest." Development 113, Supplement_2 (1991): 17–22. http://dx.doi.org/10.1242/dev.113.supplement_2.17.

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Neural crest cells migrate extensively and give rise to diverse cell types, including cells of the sensory and autonomic nervous systems. A major unanswered question concerning the neural crest is when and how the neural crest cells become determined to adopt a particular fate. We have explored the developmental potential of trunk neural crest cells in avian embryos by microinjecting a vital dye, lysinated rhodamine dextran (LRD), into individual cells within the dorsal neural tube. We find that premigratory and emigrating neural crest cells give rise to descendants with distinct phenotypes in

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2

Kulesa, P., M. Bronner-Fraser, and S. Fraser. "In ovo time-lapse analysis after dorsal neural tube ablation shows rerouting of chick hindbrain neural crest." Development 127, no. 13 (2000): 2843–52. http://dx.doi.org/10.1242/dev.127.13.2843.

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Previous analyses of single neural crest cell trajectories have suggested important roles for interactions between neural crest cells and the environment, and amongst neural crest cells. To test the relative contribution of intrinsic versus extrinsic information in guiding cells to their appropriate sites, we ablated subpopulations of premigratory chick hindbrain neural crest and followed the remaining neural crest cells over time using a new in ovo imaging technique. Neural crest cell migratory behaviors are dramatically different in ablated compared with unoperated embryos. Deviations from n

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3

Liu, J. P., and T. M. Jessell. "A role for rhoB in the delamination of neural crest cells from the dorsal neural tube." Development 125, no. 24 (1998): 5055–67. http://dx.doi.org/10.1242/dev.125.24.5055.

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The differentiation of neural crest cells from progenitors located in the dorsal neural tube appears to involve three sequential steps: the specification of premigratory neural crest cell fate, the delamination of these cells from the neural epithelium and the migration of neural crest cells in the periphery. BMP signaling has been implicated in the specification of neural crest cell fate but the mechanisms that control the emergence of neural crest cells from the neural tube remain poorly understood. To identify molecules that might function at early steps of neural crest differentiation, we

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4

Serbedzija, G. N., M. Bronner-Fraser, and S. E. Fraser. "Developmental potential of trunk neural crest cells in the mouse." Development 120, no. 7 (1994): 1709–18. http://dx.doi.org/10.1242/dev.120.7.1709.

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The availability of naturally occurring and engineered mutations in mice which affect the neural crest makes the mouse embryo an important experimental system for studying neural crest cell differentiation. Here, we determine the normal developmental potential of neural crest cells by performing in situ cell lineage analysis in the mouse by microinjecting lysinated rhodamine dextran (LRD) into individual dorsal neural tube cells in the trunk. Labeled progeny derived from single cells were found in the neural tube, dorsal root ganglia, sympathoadrenal derivatives, presumptive Schwann cells and/

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5

Raible, D. W., and J. S. Eisen. "Regulative interactions in zebrafish neural crest." Development 122, no. 2 (1996): 501–7. http://dx.doi.org/10.1242/dev.122.2.501.

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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

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6

Pakhomova, N. Yu, E. L. Strokova, A. A. Korytkin, V. V. Kozhevnikov, A. F. Gusev, and A. M. Zaydman. "History of the study of the neural crest (review)." Сибирский научный медицинский журнал 43, no. 1 (2023): 13–29. http://dx.doi.org/10.18699/ssmj20230102.

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The neural crest has long attracted the attention of evolutionary biologists and, more recently, clinical specialists, as research in recent decades has significantly expanded the boundaries of knowledge about the involvement of neural crest and neural crest cells in the development of human pathology. The neural crest and neural crest cells are a unique evolutionarily based embryonic structure. Its discovery completely changed the view of the process of embryogenesis. Knowledge of neural crest development sheds light on many of the most «established» questions of developmental biology and evo

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7

Chan, W. Y., and P. P. Tam. "A morphological and experimental study of the mesencephalic neural crest cells in the mouse embryo using wheat germ agglutinin-gold conjugate as the cell marker." Development 102, no. 2 (1988): 427–42. http://dx.doi.org/10.1242/dev.102.2.427.

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The distribution of the mesencephalic neural crest cells in the mouse embryo was studied by mapping the colonization pattern of WGA-gold labelled cells following specific labelling of the neuroectoderm and grafting of presumptive neural crest cells to orthotopic and heterotopic sites. The result showed that (1) there were concomitant changes in the morphology of the neural crest epithelium during the formation of neural crest cells, in the 4- to 7-somite-stage embryos, (2) the neural crest cells were initially confined to the lateral subectodermal region of the cranial mesenchyme and there was

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8

Hall, Brian K. "Evolutionary Origins of the Neural Crest and Neural Crest Cells." Evolutionary Biology 35, no. 4 (2008): 248–66. http://dx.doi.org/10.1007/s11692-008-9033-8.

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9

Hall, Brian K., and J. Andrew Gillis. "Incremental evolution of the neural crest, neural crest cells and neural crest-derived skeletal tissues." Journal of Anatomy 222, no. 1 (2012): 19–31. http://dx.doi.org/10.1111/j.1469-7580.2012.01495.x.

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10

Epperlein, H., D. Meulemans, M. Bronner-Fraser, H. Steinbeisser, and M. A. Selleck. "Analysis of cranial neural crest migratory pathways in axolotl using cell markers and transplantation." Development 127, no. 12 (2000): 2751–61. http://dx.doi.org/10.1242/dev.127.12.2751.

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We have examined the ability of normal and heterotopically transplanted neural crest cells to migrate along cranial neural crest pathways in the axolotl using focal DiI injections and in situ hybridization with the neural crest marker, AP-2. DiI labeling demonstrates that cranial neural crest cells migrate as distinct streams along prescribed pathways to populate the maxillary and mandibular processes of the first branchial arch, the hyoid arch and gill arches 1–4, following migratory pathways similar to those observed in other vertebrates. Another neural crest marker, the transcription factor

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11

Sechrist, J., G. N. Serbedzija, T. Scherson, S. E. Fraser, and M. Bronner-Fraser. "Segmental migration of the hindbrain neural crest does not arise from its segmental generation." Development 118, no. 3 (1993): 691–703. http://dx.doi.org/10.1242/dev.118.3.691.

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The proposed pathways of chick cranial neural crest migration and their relationship to the rhombomeres of the hindbrain have been somewhat controversial, with differing results emerging from grafting and DiI-labelling analyses. To resolve this discrepancy, we have examined cranial neural crest migratory pathways using the combination of neurofilament immunocytochemistry, which recognizes early hindbrain neural crest cells, and labelling with the vital dye, DiI. Neurofilament-positive cells with the appearance of premigratory and early-migrating neural crest cells were noted at all axial level

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12

Nakagawa, S., and M. Takeichi. "Neural crest emigration from the neural tube depends on regulated cadherin expression." Development 125, no. 15 (1998): 2963–71. http://dx.doi.org/10.1242/dev.125.15.2963.

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During the emergence of neural crest cells from the neural tube, the expression of cadherins dynamically changes. In the chicken embryo, the early neural tube expresses two cadherins, N-cadherin and cadherin-6B (cad6B), in the dorsal-most region where neural crest cells are generated. The expression of these two cadherins is, however, downregulated in the neural crest cells migrating from the neural tube; they instead begin expressing cadherin-7 (cad7). As an attempt to investigate the role of these changes in cadherin expression, we overexpressed various cadherin constructs, including N-cadhe

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13

De Bellard, Maria Elena, Yi Rao, and Marianne Bronner-Fraser. "Dual function of Slit2 in repulsion and enhanced migration of trunk, but not vagal, neural crest cells." Journal of Cell Biology 162, no. 2 (2003): 269–79. http://dx.doi.org/10.1083/jcb.200301041.

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Neural crest precursors to the autonomic nervous system form different derivatives depending upon their axial level of origin; for example, vagal, but not trunk, neural crest cells form the enteric ganglia of the gut. Here, we show that Slit2 is expressed at the entrance of the gut, which is selectively invaded by vagal, but not trunk, neural crest. Accordingly, only trunk neural crest cells express Robo receptors. In vivo and in vitro experiments demonstrate that trunk, not vagal, crest cells avoid cells or cell membranes expressing Slit2, thereby contributing to the differential ability of n

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14

Fraser, S. E., and M. Bronner-Fraser. "Migrating neural crest cells in the trunk of the avian embryo are multipotent." Development 112, no. 4 (1991): 913–20. http://dx.doi.org/10.1242/dev.112.4.913.

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Trunk neural crest cells migrate extensively and give rise to diverse cell types, including cells of the sensory and autonomic nervous systems. Previously, we demonstrated that many premigratory trunk neural crest cells give rise to descendants with distinct phenotypes in multiple neural crest derivatives. The results are consistent with the idea that neural crest cells are multipotent prior to their emigration from the neural tube and become restricted in phenotype after leaving the neural tube either during their migration or at their sites of localization. Here, we test the developmental po

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15

Erickson, C. A., and T. L. Goins. "Avian neural crest cells can migrate in the dorsolateral path only if they are specified as melanocytes." Development 121, no. 3 (1995): 915–24. http://dx.doi.org/10.1242/dev.121.3.915.

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Neural crest cells are conventionally believed to migrate arbitrarily into various pathways and to differentiate according to the environmental cues that they encounter. We present data consistent with the notion that melanocytes are directed, by virtue of their phenotype, into the dorsolateral path, whereas other neural crest derivatives are excluded. In the avian embryo, trunk neural crest cells that migrate ventrally differentiate largely into neurons and glial cells of the peripheral nervous system. Neural crest cells that migrate into the dorsolateral path become melanocytes, the pigment

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16

Nakagawa, S., and M. Takeichi. "Neural crest cell-cell adhesion controlled by sequential and subpopulation-specific expression of novel cadherins." Development 121, no. 5 (1995): 1321–32. http://dx.doi.org/10.1242/dev.121.5.1321.

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We identified two cadherins, c-cad6B and c-cad7, expressed by neural crest cells at their premigratory and migratory stages, respectively, in chicken embryos. cDNA transfection experiments showed that both were homophilic adhesion molecules, endowing cells with specific adhesiveness. During development, c-cad6B appeared in the neural fold, localizing at the future neural crest area. This expression was maintained during neural tube closure, but disappeared after neural crest cells had left the neural tube, suggesting its role in neural fold fusion and/or in the formation and maintenance of the

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17

Lallier, T., G. Leblanc, K. B. Artinger, and M. Bronner-Fraser. "Cranial and trunk neural crest cells use different mechanisms for attachment to extracellular matrices." Development 116, no. 3 (1992): 531–41. http://dx.doi.org/10.1242/dev.116.3.531.

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We have used a quantitative cell attachment assay to compare the interactions of cranial and trunk neural crest cells with the extracellular matrix (ECM) molecules fibronectin, laminin and collagen types I and IV. Antibodies to the beta 1 subunit of integrin inhibited attachment under all conditions tested, suggesting that integrins mediate neural crest cell interactions with these ECM molecules. The HNK-1 antibody against a surface carbohydrate epitope under certain conditions inhibited both cranial and trunk neural crest cell attachment to laminin, but not to fibronectin. An antiserum to alp

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18

Epstein, J. A., J. Li, D. Lang, et al. "Migration of cardiac neural crest cells in Splotch embryos." Development 127, no. 9 (2000): 1869–78. http://dx.doi.org/10.1242/dev.127.9.1869.

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Pax3 encodes a transcription factor expressed during mid-gestation in the region of the dorsal neural tube that gives rise to migrating neural crest populations. In the absence of Pax3, both humans and mice develop with neural crest defects. Homozygous Splotch embryos that lack Pax3 die by embryonic day 13.5 with cardiac defects that resemble those induced by neural crest ablation in chick models. This has led to the hypothesis that Pax3 is required for cardiac neural crest migration. However, cardiac derivatives of Pax3-expressing precursor cells have not been previously defined, and Pax3-exp

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19

Vermillion, Katie L., Kevin A. Lidberg, and Laura S. Gammill. "Cytoplasmic protein methylation is essential for neural crest migration." Journal of Cell Biology 204, no. 1 (2013): 95–109. http://dx.doi.org/10.1083/jcb.201306071.

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As they initiate migration in vertebrate embryos, neural crest cells are enriched for methylation cycle enzymes, including S-adenosylhomocysteine hydrolase (SAHH), the only known enzyme to hydrolyze the feedback inhibitor of trans-methylation reactions. The importance of methylation in neural crest migration is unknown. Here, we show that SAHH is required for emigration of polarized neural crest cells, indicating that methylation is essential for neural crest migration. Although nuclear histone methylation regulates neural crest gene expression, SAHH and lysine-methylated proteins are abundant

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20

Conway, S. J., D. J. Henderson, and A. J. Copp. "Pax3 is required for cardiac neural crest migration in the mouse: evidence from the splotch (Sp2H) mutant." Development 124, no. 2 (1997): 505–14. http://dx.doi.org/10.1242/dev.124.2.505.

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Neural crest cells originating in the occipital region of the avian embryo are known to play a vital role in formation of the septum of the cardiac outflow tract and to contribute cells to the aortic arches, thymus, thyroid and parathyroids. This ‘cardiac’ neural crest sub-population is assumed to exist in mammals, but without direct evidence. In this paper we demonstrate, using RT-PCR and in situ hybridisation, that Pax3 expression can serve as a marker of cardiac neural crest cells in the mouse embryo. Cells of this lineage were traced from the occipital neural tube, via branchial arches 3,

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21

York, Joshua R., and David W. McCauley. "The origin and evolution of vertebrate neural crest cells." Open Biology 10, no. 1 (2020): 190285. http://dx.doi.org/10.1098/rsob.190285.

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The neural crest is a vertebrate-specific migratory stem cell population that generates a remarkably diverse set of cell types and structures. Because many of the morphological, physiological and behavioural novelties of vertebrates are derived from neural crest cells, it is thought that the origin of this cell population was an important milestone in early vertebrate history. An outstanding question in the field of vertebrate evolutionary-developmental biology (evo-devo) is how this cell type evolved in ancestral vertebrates. In this review, we briefly summarize neural crest developmental gen

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Kulesa, P. M., and S. E. Fraser. "In ovo time-lapse analysis of chick hindbrain neural crest cell migration shows cell interactions during migration to the branchial arches." Development 127, no. 6 (2000): 1161–72. http://dx.doi.org/10.1242/dev.127.6.1161.

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Hindbrain neural crest cells were labeled with DiI and followed in ovo using a new approach for long-term time-lapse confocal microscopy. In ovo imaging allowed us to visualize neural crest cell migration 2–3 times longer than in whole embryo explant cultures, providing a more complete picture of the dynamics of cell migration from emergence at the dorsal midline to entry into the branchial arches. There were aspects of the in ovo neural crest cell migration patterning which were new and different. Surprisingly, there was contact between neural crest cell migration streams bound for different

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Dottori, Mirella, Michael K. Gross, Patricia Labosky, and Martyn Goulding. "The winged-helix transcription factor Foxd3 suppresses interneuron differentiation and promotes neural crest cell fate." Development 128, no. 21 (2001): 4127–38. http://dx.doi.org/10.1242/dev.128.21.4127.

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The neural crest is a migratory cell population that gives rise to multiple cell types in the vertebrate embryo. The intrinsic determinants that segregate neural crest cells from multipotential dorsal progenitors within the neural tube are poorly defined. In this study, we show that the winged helix transcription factor Foxd3 is expressed in both premigratory and migratory neural crest cells. Foxd3 is genetically downstream of Pax3 and is not expressed in regions of Pax3 mutant mice that lack neural crest, implying that Foxd3 may regulate aspects of the neural crest differentiation program. We

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Serbedzija, G. N., M. Bronner-Fraser, and S. E. Fraser. "A vital dye analysis of the timing and pathways of avian trunk neural crest cell migration." Development 106, no. 4 (1989): 809–16. http://dx.doi.org/10.1242/dev.106.4.809.

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To permit a more detailed analysis of neural crest cell migratory pathways in the chick embryo, neural crest cells were labelled with a nondeleterious membrane intercalating vital dye, DiI. All neural tube cells with endfeet in contact with the lumen, including premigratory neural crest cells, were labelled by pressure injecting a solution of DiI into the lumen of the neural tube. When assayed one to three days later, migrating neural crest cells, motor axons, and ventral root cells were the only cells types external to the neural tube labelled with DiI. During the neural crest cell migratory

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BAREMBAUM, MEYER, and MARIANNE BRONNER-FRASER. "A novel spalt gene expressed in branchial arches affects the ability of cranial neural crest cells to populate sensory ganglia." Neuron Glia Biology 1, no. 1 (2004): 57–63. http://dx.doi.org/10.1017/s1740925x04000080.

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Cranial neural crest cells differentiate into diverse derivatives including neurons and glia of the cranial ganglia, and cartilage and bone of the facial skeleton. Here, we explore the function of a novel transcription factor of the spalt family that might be involved in early cell-lineage decisions of the avian neural crest. The chicken spalt4 gene (csal4) is expressed in the neural tube, migrating neural crest, branchial arches and, transiently, in the cranial ectoderm. Later, it is expressed in the mesectodermal, but not neuronal or glial, derivatives of midbrain and hindbrain neural crest.

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Mackie, E. J., R. P. Tucker, W. Halfter, R. Chiquet-Ehrismann, and H. H. Epperlein. "The distribution of tenascin coincides with pathways of neural crest cell migration." Development 102, no. 1 (1988): 237–50. http://dx.doi.org/10.1242/dev.102.1.237.

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The distribution of the extracellular matrix (ECM) glycoprotein, tenascin, has been compared with that of fibronectin in neural crest migration pathways of Xenopus laevis, quail and rat embryos. In all species studied, the distribution of tenascin, examined by immunohistochemistry, was more closely correlated with pathways of migration than that of fibronectin, which is known to be important for neural crest migration. In Xenopus laevis embryos, anti-tenascin stained the dorsal fin matrix and ECM along the ventral route of migration, but not the ECM found laterally between the ectoderma and so

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Paratore, Christian, Derk E. Goerich, Ueli Suter, Michael Wegner, and Lukas Sommer. "Survival and glial fate acquisition of neural crest cells are regulated by an interplay between the transcription factor Sox10 and extrinsic combinatorial signaling." Development 128, no. 20 (2001): 3949–61. http://dx.doi.org/10.1242/dev.128.20.3949.

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The transcription factor Sox10 is required for proper development of various neural crest-derived cell types. Several lineages including melanocytes, autonomic and enteric neurons, and all subtypes of peripheral glia are missing in mice homozygous for Sox10 mutations. Moreover, haploinsufficiency of Sox10 results in neural crest defects that cause Waardenburg/Hirschsprung disease in humans. We provide evidence that the cellular basis to these phenotypes is likely to be a requirement for Sox10 by neural crest stem cells before lineage segregation. Cell death is increased in undifferentiated, po

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Smith-Thomas, L. C., and J. W. Fawcett. "Expression of Schwann cell markers by mammalian neural crest cells in vitro." Development 105, no. 2 (1989): 251–62. http://dx.doi.org/10.1242/dev.105.2.251.

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During embryonic development, neural crest cells differentiate into a wide variety of cell types including Schwann cells of the peripheral nervous system. In order to establish when neural crest cells first start to express a Schwann cell phenotype immunocytochemical techniques were used to examine rat premigratory neural crest cell cultures for the presence of Schwann cell markers. Cultures were fixed for immunocytochemistry after culture periods ranging from 1 to 24 days. Neural crest cells were identified by their morphology and any neural tube cells remaining in the cultures were identifie

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Trainor, Paul A., Dorothy Sobieszczuk, David Wilkinson, and Robb Krumlauf. "Signalling between the hindbrain and paraxial tissues dictates neural crest migration pathways." Development 129, no. 2 (2002): 433–42. http://dx.doi.org/10.1242/dev.129.2.433.

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Cranial neural crest cells are a pluripotent population of cells derived from the neural tube that migrate into the branchial arches to generate the distinctive bone, connective tissue and peripheral nervous system components characteristic of the vertebrate head. The highly conserved segmental organisation of the vertebrate hindbrain plays an important role in pattering the pathways of neural crest cell migration and in generating the distinct or separate streams of crest cells that form unique structures in each arch. We have used focal injections of DiI into the developing mouse hindbrain i

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Selleck, M. A., and M. Bronner-Fraser. "Origins of the avian neural crest: the role of neural plate-epidermal interactions." Development 121, no. 2 (1995): 525–38. http://dx.doi.org/10.1242/dev.121.2.525.

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We have investigated the lineage and tissue interactions that result in avian neural crest cell formation from the ectoderm. Presumptive neural plate was grafted adjacent to non-neural ectoderm in whole embryo culture to examine the role of tissue interactions in ontogeny of the neural crest. Our results show that juxtaposition of non-neural ectoderm and presumptive neural plate induces the formation of neural crest cells. Quail/chick recombinations demonstrate that both the prospective neural plate and the prospective epidermis can contribute to the neural crest. When similar neural plate/epi

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Artinger, K. B., A. B. Chitnis, M. Mercola, and W. Driever. "Zebrafish narrowminded suggests a genetic link between formation of neural crest and primary sensory neurons." Development 126, no. 18 (1999): 3969–79. http://dx.doi.org/10.1242/dev.126.18.3969.

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In the developing vertebrate nervous system, both neural crest and sensory neurons form at the boundary between non-neural ectoderm and the neural plate. From an in situ hybridization based expression analysis screen, we have identified a novel zebrafish mutation, narrowminded (nrd), which reduces the number of early neural crest cells and eliminates Rohon-Beard (RB) sensory neurons. Mosaic analysis has shown that the mutation acts cell autonomously suggesting that nrd is involved in either the reception or interpretation of signals at the lateral neural plate boundary. Characterization of the

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Bronner-Fraser, M. "Alterations in neural crest migration by a monoclonal antibody that affects cell adhesion." Journal of Cell Biology 101, no. 2 (1985): 610–17. http://dx.doi.org/10.1083/jcb.101.2.610.

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The possible role of a 140-kD cell surface complex in neural crest adhesion and migration was examined using a monoclonal antibody JG22, first described by Greve and Gottlieb (1982, J. Cell. Biochem. 18:221-229). The addition of JG22 to neural crest cells in vitro caused a rapid change in morphology of cells plated on either fibronectin or laminin substrates. The cells became round and phase bright, often detaching from the dish or forming aggregates of rounded cells. Other tissues such as somites, notochords, and neural tubes were unaffected by the antibody in vitro even though the JG22 antig

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Sechrist, J., M. A. Nieto, R. T. Zamanian, and M. Bronner-Fraser. "Regulative response of the cranial neural tube after neural fold ablation: spatiotemporal nature of neural crest regeneration and up-regulation of Slug." Development 121, no. 12 (1995): 4103–15. http://dx.doi.org/10.1242/dev.121.12.4103.

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After unilateral ablation of the avian cranial neural folds, the remaining neuroepithelial cells are able to replace the missing neural crest population (Scherson et al., 1993). Here, we characterize the cellular and molecular nature of this regulative response by defining: (1) the time and location of neural crest cell production by the neuroepithelium; (2) rostrocaudal axial differences in the regulative response; and (3) the onset of expression of Slug, a transcription factor present in premigratory and migrating neural crest cells. Using DiI and HNK-1 antibody labeling techniques, we find

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Erickson, Carol A. "Control of pathfinding by the avian trunk neural crest." Development 103, Supplement (1988): 63–80. http://dx.doi.org/10.1242/dev.103.supplement.63.

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We have determined the pathways taken by the trunk neural crest of quail and examined the parameters that control these patterns of dispersion. Using antibodies that recognize migratory neural crest cells (HNK-1), we have found that the crest cells take three primary pathways: (1) between the ectoderm and somites, (2) within the intersomitic space and (3) through the anterior somite along the basal surface of the myotome. The parameters controlling dispersion patterns of neural crest cells are several. The pathways are filled with at least two adhesive molecules, laminin and fibronectin, to wh

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Birgbauer, E., J. Sechrist, M. Bronner-Fraser, and S. Fraser. "Rhombomeric origin and rostrocaudal reassortment of neural crest cells revealed by intravital microscopy." Development 121, no. 4 (1995): 935–45. http://dx.doi.org/10.1242/dev.121.4.935.

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Neural crest cell migration in the hindbrain is segmental, with prominent streams of migrating cells adjacent to rhombomeres (r) r2, r4 and r6, but not r3 or r5. This migratory pattern cannot be explained by the failure of r3 and r5 to produce neural crest, since focal injections of the lipophilic dye, DiI, into the neural folds clearly demonstrate that all rhombomeres produce neural crest cells. Here, we examine the dynamics of hindbrain neural crest cell emigration and movement by iontophoretically injecting DiI into small numbers of cells. The intensely labeled cells and their progeny were

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Sarkar, Sanjukta, Anita Petiot, Andrew Copp, Patrizia Ferretti, and Peter Thorogood. "FGF2 promotes skeletogenic differentiation of cranial neural crest cells." Development 128, no. 11 (2001): 2143–52. http://dx.doi.org/10.1242/dev.128.11.2143.

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The cranial neural crest gives rise to most of the skeletal tissues of the skull. Matrix-mediated tissue interactions have been implicated in the skeletogenic differentiation of crest cells, but little is known of the role that growth factors might play in this process. The discovery that mutations in fibroblast growth factor receptors (FGFRs) cause the major craniosynostosis syndromes implicates FGF-mediated signalling in the skeletogenic differentiation of the cranial neural crest. We now show that, in vitro, mesencephalic neural crest cells respond to exogenous FGF2 in a dose-dependent mann

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Xu, X., W. E. I. Li, G. Y. Huang, et al. "Modulation of mouse neural crest cell motility by N-cadherin and connexin 43 gap junctions." Journal of Cell Biology 154, no. 1 (2001): 217–30. http://dx.doi.org/10.1083/jcb.200105047.

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Connexin 43 (Cx43α1) gap junction has been shown to have an essential role in mediating functional coupling of neural crest cells and in modulating neural crest cell migration. Here, we showed that N-cadherin and wnt1 are required for efficient dye coupling but not for the expression of Cx43α1 gap junctions in neural crest cells. Cell motility was found to be altered in the N-cadherin–deficient neural crest cells, but the alterations were different from that elicited by Cx43α1 deficiency. In contrast, wnt1-deficient neural crest cells showed no discernible change in cell motility. These observ

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Weigele, Jochen, and Brenda L. Bohnsack. "Genetics Underlying the Interactions between Neural Crest Cells and Eye Development." Journal of Developmental Biology 8, no. 4 (2020): 26. http://dx.doi.org/10.3390/jdb8040026.

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The neural crest is a unique, transient stem cell population that is critical for craniofacial and ocular development. Understanding the genetics underlying the steps of neural crest development is essential for gaining insight into the pathogenesis of congenital eye diseases. The neural crest cells play an under-appreciated key role in patterning the neural epithelial-derived optic cup. These interactions between neural crest cells within the periocular mesenchyme and the optic cup, while not well-studied, are critical for optic cup morphogenesis and ocular fissure closure. As a result, micro

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Leslie, Mitch. "Sip1 liberates neural crest cells." Journal of Cell Biology 203, no. 5 (2013): 712. http://dx.doi.org/10.1083/jcb.2035iti3.

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Hines, P. J. "Versatile embryonic neural crest cells." Science 352, no. 6293 (2016): 1530. http://dx.doi.org/10.1126/science.352.6293.1530-a.

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VanHook, Annalisa M. "Contact repels neural crest cells." Science Signaling 8, no. 392 (2015): ec246-ec246. http://dx.doi.org/10.1126/scisignal.aad3230.

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Sieber-Blum, Maya. "Cardiac neural crest stem cells." Anatomical Record 276A, no. 1 (2003): 34–42. http://dx.doi.org/10.1002/ar.a.10132.

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Kos, R., M. V. Reedy, R. L. Johnson, and C. A. Erickson. "The winged-helix transcription factor FoxD3 is important for establishing the neural crest lineage and repressing melanogenesis in avian embryos." Development 128, no. 8 (2001): 1467–79. http://dx.doi.org/10.1242/dev.128.8.1467.

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The winged-helix or forkhead class of transcription factors has been shown to play important roles in cell specification and lineage segregation. We have cloned the chicken homolog of FoxD3, a member of the winged-helix class of transcription factors, and analyzed its expression. Based on its expression in the dorsal neural tube and in all neural crest lineages except the late-emigrating melanoblasts, we predicted that FoxD3 might be important in the segregation of the neural crest lineage from the neural epithelium, and for repressing melanogenesis in early-migrating neural crest cells. Misex

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Scherson, T., G. Serbedzija, S. Fraser, and M. Bronner-Fraser. "Regulative capacity of the cranial neural tube to form neural crest." Development 118, no. 4 (1993): 1049–62. http://dx.doi.org/10.1242/dev.118.4.1049.

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In avian embryos, cranial neural crest cells emigrate from the dorsal midline of the neural tube shortly after neural tube closure. Previous lineage analyses suggest that the neural crest is not a pre-segregated population of cells within the neural tube; instead, a single progenitor in the dorsal neural tube can contribute to neurons in both the central and the peripheral nervous systems (Bronner-Fraser and Fraser, 1989 Neuron 3, 755–766). To explore the relationship between the ‘premigratory’ neural crest cells and the balance of the cells in the neural tube in the midbrain and hindbrain reg

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Duband, J. L., and J. P. Thiery. "Spatial and temporal distribution of vinculin and talin in migrating avian neural crest cells and their derivatives." Development 108, no. 3 (1990): 421–33. http://dx.doi.org/10.1242/dev.108.3.421.

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Neural crest cells express different adhesion modes at each phase of their development starting with their separation from the neural tube, followed by migration along definite pathways throughout the embryo, and finally to settlement and differentiation in elected embryonic regions. In order to determine possible changes in the cytoskeleton organization and function during these processes, we have studied the in situ distribution of two major cytoskeleton-associated elements involved in the membrane anchorage of actin microfilaments, i.e. vinculin and talin, during the ontogeny of the neural

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Monteagudo de la Rosa, M., M. González-Santander Martínez, G. Martinez Cuadrado, and R. González Santander. "Immunohistochemical Identification and Electron Microscopic Study on Early Migrating Neural Crest Cells in the Chick Embryo." Microscopy and Microanalysis 3, S2 (1997): 177–78. http://dx.doi.org/10.1017/s1431927600007777.

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Just after neural fold fusion to form the neural tube, neural crest cells detach from the neural crest, a transient structure located in the dorsal region of the neural tube. Neural crest cells migrate and differentiate into many structures and cells. But the underlying controls of this detachment and initiation of emigration are unknown. Neural crest cells are usually not morphologically distinct from the adjacent neural epithelium (neural tube) and epidermal ectoderm (epiblast) flanking them. We are combining morphological and immunohistochemical approaches to study neural crest cells in the

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Krull, C. E., A. Collazo, S. E. Fraser, and M. Bronner-Fraser. "Segmental migration of trunk neural crest: time-lapse analysis reveals a role for PNA-binding molecules." Development 121, no. 11 (1995): 3733–43. http://dx.doi.org/10.1242/dev.121.11.3733.

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Trunk neural crest cells migrate through the somites in a striking segmental fashion, entering the rostral but not caudal sclerotome, via cues intrinsic to the somites. Attempts to define the molecular bases of these cues have been hampered by the lack of an accessible assay system. To examine trunk neural crest migration over time and to perturb candidate guiding molecules, we have developed a novel explant preparation. Here, we demonstrate that trunk regions of the chicken embryo, placed in explant culture, continue to develop apparently normally for 2 days. Neural crest cells, recognized by

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Graham, A., I. Heyman, and A. Lumsden. "Even-numbered rhombomeres control the apoptotic elimination of neural crest cells from odd-numbered rhombomeres in the chick hindbrain." Development 119, no. 1 (1993): 233–45. http://dx.doi.org/10.1242/dev.119.1.233.

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Neural crest cells originate at three discontinuous levels along the rostrocaudal axis of the chick rhombencephalon, centred on rhombomeres 1 and 2, 4 and 6, respectively. These are separated by the odd-numbered rhombomeres r3 and r5 which are depleted of migratory neural crest cells. Here we show elevated levels of apoptosis in the dorsal midline of r3 and r5, immediately following the formation of these rhombomeres at the developmental stage (10–12) when neural crest cells would be expected to emerge at these neuraxial levels. These regions are also marked by their expression of members of t

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Saldivar, J. R., J. W. Sechrist, C. E. Krull, S. Ruffins, and M. Bronner-Fraser. "Dorsal hindbrain ablation results in rerouting of neural crest migration and changes in gene expression, but normal hyoid development." Development 124, no. 14 (1997): 2729–39. http://dx.doi.org/10.1242/dev.124.14.2729.

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Our previous studies have shown that hindbrain neural tube cells can regulate to form neural crest cells for a limited time after neural fold removal (Scherson, T., Serbedzija, G., Fraser, S. E. and Bronner-Fraser, M. (1993). Development 188, 1049–1061; Sechrist, J., Nieto, M. A., Zamanian, R. T. and Bronner-Fraser, M. (1995). Development 121, 4103–4115). In the present study, we ablated the dorsal hindbrain at later stages to examine possible alterations in migratory behavior and/or gene expression in neural crest populations rostral and caudal to the operated region. The results were compare

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Saldivar, J. R., C. E. Krull, R. Krumlauf, L. Ariza-McNaughton, and M. Bronner-Fraser. "Rhombomere of origin determines autonomous versus environmentally regulated expression of Hoxa-3 in the avian embryo." Development 122, no. 3 (1996): 895–904. http://dx.doi.org/10.1242/dev.122.3.895.

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We have investigated the pattern and regulation of Hoxa3 expression in the hindbrain and associated neural crest cells in the chick embryo, using whole mount in situ hybridization in conjunction with DiI labeling of neural crest cells and microsurgical manipulations. Hoxa3 is expressed in the neural plate and later in the neural tube with a rostral border of expression corresponding to the boundary between rhombomeres (r) 4 and 5. Initial expression is diffuse and becomes sharp after boundary formation. Hoxa3 exhibits uniform expression within r5 after formation of rhombomeric borders. Cell ma

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