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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 multiple neural crest derivatives. These 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 emigration from the neural tube either during their migration or at their sites of localization. To determine whether neural crest cells become restricted during their migration, we have microinjected individual trunk neural crest cells with dye shortly after they leave the neural tube or as they migrate through the somite. We find that a majority of the clones derived from migrating neural crest cells appear to be multipotent; individual migrating neural crest cells gave rise to both sensory and sympathetic neurons, as well as cells with the morphological characteristics of Schwann cells, and other nonneuronal cells. Even those clones contributing to only one neural crest derivative often contained both neurofilament-positive and neurofilament-negative cells. These data demonstrate that migrating trunk neural crest cells, like their premigratory progenitors, can be multipotent. They give rise to cells in multiple neural crest derivatives and contribute to both neuronal and non-neuronal elements within a given derivative. Thus, restriction of neural crest cell fate must occur relatively late in migration or at the final destinations.
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 normal migration appear either shortly after cells emerge from the neural tube or en route to the branchial arches, areas where cell-cell interactions typically occur between neural crest cells in normal embryos. Unlike the persistent, directed trajectories in normal embryos, neural crest cells frequently change direction and move somewhat chaotically after ablation. In addition, the migration of neural crest cells in collective chains, commonly observed in normal embryos, was severely disrupted. Hindbrain neural crest cells have the capacity to reroute their migratory pathways and thus compensate for missing neural crest cells after ablation of neighboring populations. Because the alterations in neural crest cell migration are most dramatic in regions that would normally foster cell-cell interactions, the trajectories reported here argue that cell-cell interactions have a key role in the shaping of the neural crest migration.
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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 performed a PCR-based screen for genes induced by BMPs in chick neural plate cells. We describe the cloning and characterization of one gene obtained from this screen, rhoB, a member of the rho family GTP-binding proteins. rhoB is expressed in the dorsal neural tube and its expression persists transiently in migrating neural crest cells. BMPs induce the neural expression of rhoB but not the more widely expressed rho family member, rhoA. Inhibition of rho activity by C3 exotoxin prevents the delamination of neural crest cells from neural tube explants but has little effect on the initial specification of premigratory neural crest cell fate or on the later migration of neural crest cells. These results suggest that rhoB has a role in the delamination of neural crest cells from the dorsal neural tube.
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/or pigment cells. Most embryos contained labeled cells both in the neural tube and at least one neural crest derivative, and numerous clones contributed to multiple neural crest derivatives. The time of injection influenced the derivatives populated by the labeled cells. Injections at early stages of migration yielded labeled progeny in both dorsal and ventral neural crest derivatives, whereas those performed at later stages had labeled cells only in more dorsal neural crest derivatives, such as dorsal root ganglion and presumptive pigment cells. The results suggest that in the mouse embryo: (1) there is a common precursor for neural crest and neural tube cells; (2) some neural crest cells are multipotent; and (3) the timing of emigration influences the range of possible neural crest derivatives.
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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 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.
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 evolution. Our article will reflect on the historical stages of the discovery and study of the neural crest and the impact of this discovery on entrenched ideas about germ layer specificity and the theory of germ layers – the reasoning of the neural crest as the fourth germ layer. The aim of this review is to describe the history of the discovery and study of neural crest and neural crest cells based on an analysis of the literature. In writing this article, an analysis of the scientific literature was conducted using the search terms «neural crest», «neural crest cells», «neural crest cell morphology», «germinal layers» and «embryonic development» in the computer databases PubMed, Scopus, Web of Science, and eLibrary. The depth of the analytical search corresponds to the period of the discovery of the neural crest and the first mention of the neural crest as an embryonic morphological structure in the scientific literature. The information presented confirms the high interest of research scientists and clinical specialists in the study of neural crest and neural crest cells. The involvement of neural crest cells in the formation of somatic and musculoskeletal pathologies has received particular attention in recent decades. The literature sources are represented by 169 full-text manuscripts and monographs mainly in English. Conclusions. Neural crest and neural crest cells are unique evolutionary structures. Regularities of formation, reasons which condition migration, differentiation, interaction of neural crest cells with other structures during embryogenesis as well as their potential, which is realized in postnatal period, continue to be the subject of research up to now.
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 minimal mixing with the paraxial mesoderm underneath the neural plate, (3) labelled cells from the presumptive crest region colonized the lateral cranio-facial mesenchyme, the developing trigeminal ganglion and the pharyngeal arch, (4) the formation of neural crest cells was facilitated by the focal disruption of the basal lamina and the cell-cell interaction specific to the neural crest site and (5) the trigeminal ganglion was colonized not only by neural crest cells but also by cells from the ectodermal placode.
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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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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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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 AP-2, is expressed by premigratory neural crest cells within the neural folds and migrating neural crest cells en route to and within the branchial arches. Rotations of the cranial neural folds suggest that premigratory neural crest cells are not committed to a specific branchial arch fate, but can compensate when displaced short distances from their targets by migrating to a new target arch. In contrast, when cells are displaced far from their original location, they appear unable to respond appropriately to their new milieu such that they fail to migrate or appear to migrate randomly. When trunk neural folds are grafted heterotopically into the head, trunk neural crest cells migrate in a highly disorganized fashion and fail to follow normal cranial neural crest pathways. Importantly, we find incorporation of some trunk cells into branchial arch cartilage despite the random nature of their migration. This is the first demonstration that trunk neural crest cells can form cartilage when transplanted to the head. Our results indicate that, although cranial and trunk neural crest cells have inherent differences in ability to recognize migratory pathways, trunk neural crest can differentiate into cranial cartilage when given proper instructive cues.
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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 levels of the hindbrain. At slightly later stages, neural crest cell migration in this region appeared segmented, with no neural crest cells obvious in the mesenchyme lateral to rhombomere 3 (r3) and between the neural tube and the otic vesicle lateral to r5. Focal injections of DiI at the levels of r3 and r5 demonstrated that both of these rhombomeres generated neural crest cells. The segmental distribution of neural crest cells resulted from the DiI-labelled cells that originated in r3 and r5 deviating rostrally or caudally and failing to enter the adjacent preotic mesoderm or otic vesicle region. The observation that neural crest cells originating from r3 and r5 avoided specific neighboring domains raises the intriguing possibility that, as in the trunk, extrinsic factors play a major role in the axial patterning of the cranial neural crest and the neural crest-derived peripheral nervous system.
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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-cadherin, cad7, and a dominant negative N-cadherin (cN390), in neural crest-generating cells. This was achieved by injecting adenoviral expression vectors encoding these molecules into the lumen of the closing neural tube of chicken embryos at stage 14. In neural tubes injected with the viruses, efficient infection was observed at the neural crest-forming area, resulting in the ectopic cadherin expression also in migrating neural crest cells. Notably, the distribution of neural crest cells with the ectopic cadherins changed depending on which constructs were expressed. Many crest cells failed to escape from the neural tube when N-cadherin or cad7 was overexpressed. Moreover, none of the cells with these ectopic cadherins migrated along the dorsolateral (melanocyte) pathway. When these samples were stained for Mitf, an early melanocyte marker, positive cells were found accumulated within the neural tube, suggesting that the failure of their migration was not due to differentiation defects. In contrast to these phenomena, cells expressing non-functional cadherins exhibited a normal migration pattern. Thus, the overexpression of a neuroepithelial cadherin (N-cadherin) and a crest cadherin (cad7) resulted in the same blocking effect on neural crest segregation from neuroepithelial cells, especially for melanocyte precursors. These findings suggest that the regulation of cadherin expression or its activity at the neural crest-forming area plays a critical role in neural crest emigration from the neural tube.
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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 neural crest populations to invade and innervate the gut. Conversely, exposure to soluble Slit2 significantly increases the distance traversed by trunk neural crest cells. These results suggest that Slit2 can act bifunctionally, both repulsing and stimulating the motility of trunk neural crest cells.
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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 potential of migrating trunk neural crest cells by microinjecting a vital dye, lysinated rhodamine dextran (LRD), into individual cells as they migrate through the somite. By two days after injection, the LRD-labelled clones contained from 2 to 67 cells, which were distributed unilaterally in all embryos. Most clones were confined to a single segment, though a few contributed to sympathetic ganglia over two segments. A majority of the clones gave rise to cells in multiple neural crest derivatives. Individual migrating neural crest cells gave rise to both sensory and sympathetic neurons (neurofilament-positive), as well as cells with the morphological characteristics of Schwann cells, and other non-neuronal cells (both neurofilament-negative). Even those clones contributing to only one neural crest derivative often contained both neurofilament-positive and neurofilament-negative cells. Our data demonstrate that migrating trunk neural crest cells can be multipotent, giving rise to cells in multiple neural crest derivatives, and contributing to both neuronal and non-neuronal elements within a given derivative.(ABSTRACT TRUNCATED AT 250 WORDS)
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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 cells of the skin. Neural crest cells destined for the dorsolateral path are delayed in their migration until at least 24 hours after migration commences ventrally. Previous studies have suggested that invasion into the dorsolateral path is dependent upon a change in the migratory environment. A complementary possibility is that as neural crest cells differentiate into melanocytes they acquire the ability to take this pathway. When quail neural crest cells that have been grown in culture for 12 hours are labeled with Fluoro-gold and then grafted into the early migratory pathway at the thoracic level, they migrate only ventrally and are coincident with the host neural crest. When fully differentiated melanocytes (96 hours old) are back-grafted under identical conditions, however, they enter the dorsolateral path and invade the ectoderm at least one day prior to the host neural crest. Likewise, neural crest cells that have been cultured for at least 20 hours and are enriched in melanoblasts immediately migrate in the dorsolateral path, in addition to the ventral path, when back-grafted into the thoracic level. A population of neural crest cells depleted of melanoblasts--crest cells derived from the branchial arches--are not able to invade the dorsolateral path, suggesting that only pigment cells or their precursors are able to take this migratory route. These results suggest that as neural crest cells differentiate into melanocytes they can exploit the dorsolateral path immediately. Even when 12-hour crest cells are grafted into stage 19–21 embryos at an axial level where host crest are invading the dorsolateral path, these young neural crest cells do not migrate dorsolaterally. Conversely, melanoblasts or melanocytes grafted under the same circumstances are found in the ectoderm. These latter results suggest that during normal development neural crest cells must be specified, if not already beginning to differentiate, as melanocytes in order to take this path.(ABSTRACT TRUNCATED AT 400 WORDS)
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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 presumptive neural crest domain in the neural plate/tube. Crest cells emerging from the neural tube lost c-cad6B, and a subpopulation of them began to express c-cad7. This subpopulation-specific expression of c-cad7 persisted during their migration. The migrating c-cad7-positive cells clustered together, and eventually populated restricted regions including the dorsal and ventral roots but very little ganglia. The latter was populated with N-cadherin-positive crest cells. Migrating neural crest cells expressed alpha- and beta-catenin at cell-cell contacts, indicating that their cadherins are functioning. These results suggest that the migrating crest cells are grouped into subpopulations expressing different cadherins. The cadherin-mediated specific interaction between crest cells likely plays a role in intercellular signaling between homotypic cells as well as in sorting of heterotypic cells.
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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 alpha 1 intergrin inhibited attachment of trunk, but not cranial, neural crest cells to laminin and collagen type I, though interactions with fibronectin or collagen type IV were unaffected. The surface properties of trunk and cranial neural crest cells differed in several ways. First, trunk neural crest cells attached to collagen types I and IV, but cranial neural crest cells did not. Second, their divalent cation requirements for attachment to ECM molecules differed. For fibronectin substrata, trunk neural crest cells required divalent cations for attachment, whereas cranial neural crest cells bound in the absence of divalent cations. However, cranial neural crest cells lost this cation-independent attachment after a few days of culture. For laminin substrata, trunk cells used two integrins, one divalent cation-dependent and the other divalent cation-independent (Lallier, T. E. and Bronner-Fraser, M. (1991) Development 113, 1069–1081). In contrast, cranial neural crest cells attached to laminin using a single, divalent cation-dependent receptor system. Immunoprecipitations and immunoblots of surface labelled neural crest cells with HNK-1, alpha 1 integrin and beta 1 integrin antibodies suggest that cranial and trunk neural crest cells possess biochemically distinct integrins. Our results demonstrate that cranial and trunk cells differ in their mechanisms of adhesion to selected ECM components, suggesting that they are non-overlapping populations of cells with regard to their adhesive properties.
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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-expressing cells within the heart have not been well demonstrated. Hence, the precise role of Pax3 during cardiac development remains unclear. Here, we use a Cre-lox method to fate map Pax3-expressing neural crest precursors to the cardiac outflow tract. We show that although Pax3 itself is extinguished prior to neural crest populating the heart, derivatives of these precursors contribute to the aorticopulmonary septum. We further show that neural crest cells are found in the outflow tract of Splotch embryos, albeit in reduced numbers. This indicates that contrary to prior reports, Pax3 is not required for cardiac neural crest migration. Using a neural tube explant culture assay, we demonstrate that neural crest cells from Splotch embryos show normal rates of proliferation but altered migratory characteristics. These studies suggest that Pax3 is required for fine tuning the migratory behavior of the cardiac neural crest cells while it is not essential for neural crest migration.
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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 in the cytoplasm of migratory neural crest cells. Proteomic profiling of cytoplasmic, lysine-methylated proteins from migratory neural crest cells identified 182 proteins, several of which are cytoskeleton related. A methylation-resistant form of one of these proteins, the actin-binding protein elongation factor 1 alpha 1 (EF1α1), blocks neural crest migration. Altogether, these data reveal a novel and essential role for post-translational nonhistone protein methylation during neural crest migration and define a previously unknown requirement for EF1α1 methylation in migration.
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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, 4 and 6, into the aortic sac and aorto-pulmonary outflow tract. Confirmation that these Pax3-positive cells are indeed cardiac neural crest is provided by experiments in which hearts were deprived of a source of colonising neural crest, by organ culture in vitro, with consequent lack of up-regulation of Pax3. Occipital neural crest cell outgrowths in vitro were also shown to express Pax3. Mutation of Pax3, as occurs in the splotch (Sp2H) mouse, results in development of conotruncal heart defects including persistent truncus arteriosus. Homozygotes also exhibit defects of the aortic arches, thymus, thyroid and parathyroids. Pax3-positive neural crest cells were found to emigrate from the occipital neural tube of Sp2H/Sp2H embryos in a relatively normal fashion, but there was a marked deficiency or absence of neural crest cells traversing branchial arches 3, 4 and 6, and entering the cardiac outflow tract. This decreased expression of Pax3 in Sp2H/Sp2H embryos was not due to down-regulation of Pax3 in neural crest cells, as use of independent neural crest markers, Hoxa-3, CrabpI, Prx1, Prx2 and c-met also revealed a deficiency of migrating cardiac neural crest cells in homozygous embryos. This work demonstrates the essential role of the cardiac neural crest in formation of the heart and great vessels in the mouse and, furthermore, shows that Pax3 function is required for the cardiac neural crest to complete its migration to the developing heart.
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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 genetics in vertebrates, focusing in particular on the gene regulatory interactions instructing their early formation within and migration from the dorsal neural tube. We then discuss how studies searching for homologues of neural crest cells in invertebrate chordates led to the discovery of neural crest-like cells in tunicates and the potential implications this has for tracing the pre-vertebrate origins of the neural crest population. Finally, we synthesize this information to propose a model to explain the origin of neural crest cells. We suggest that at least some of the regulatory components of early stages of neural crest development long pre-date vertebrate origins, perhaps dating back to the last common bilaterian ancestor. These components, originally directing neuroectodermal patterning and cell migration, served as a gene regulatory ‘scaffold' upon which neural crest-like cells with limited migration and potency evolved in the last common ancestor of tunicates and vertebrates. Finally, the acquisition of regulatory programmes controlling multipotency and long-range, directed migration led to the transition from neural crest-like cells in invertebrate chordates to multipotent migratory neural crest in the first vertebrates.
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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.
Full textAbstract:
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 branchial arches. This cell-cell contact occurred in the region lateral to the otic vesicle, where neural crest cells within the distinct streams diverted from their migration pathways into the branchial arches and instead migrated around the otic vesicle to establish a contact between streams. Some individual neural crest cells did appear to cross between the streams, but there was no widespread mixing. Analysis of individual cell trajectories showed that neural crest cells emerge from all rhombomeres (r) and sort into distinct exiting streams adjacent to the even-numbered rhombomeres. Neural crest cell migration behaviors resembled the wide diversity seen in whole embryo chick explants, including chain-like cell arrangements; however, average in ovo cell speeds are as much as 70% faster. To test to what extent neural crest cells from adjoining rhombomeres mix along migration routes and within the branchial arches, separate groups of premigratory neural crest cells were labeled with DiI or DiD. Results showed that r6 and r7 neural crest cells migrated to the same spatial location within the fourth branchial arch. The diversity of migration behaviors suggests that no single mechanism guides in ovo hindbrain neural crest cell migration into the branchial arches. The cell-cell contact between migration streams and the co-localization of neural crest cells from adjoining rhombomeres within a single branchial arch support the notion that the pattern of hindbrain neural crest cell migration emerges dynamically with cell-cell communication playing an important guidance role.
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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.
Full textAbstract:
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 show that misexpression of Foxd3 in the chick neural tube promotes a neural crest-like phenotype and suppresses interneuron differentiation. Cells that ectopically express Foxd3 upregulate HNK1 and Cad7, delaminate and emigrate from the neural tube at multiple dorsoventral levels. Foxd3 does not induce Slug and RhoB, nor is its ability to promote a neural crest-like phenotype enhanced by co-expression of Slug. Together these results suggest Foxd3 can function independently of Slug and RhoB to promote the development of neural crest cells from neural tube progenitors.
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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.
Full textAbstract:
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 phase, distinctly labelled cells were found along: (1) a dorsolateral pathway, under the epidermis, as well adjacent to and intercalating through the dermamyotome; and (2) a ventral pathway, through the rostral portion of each sclerotome and around the dorsal aorta as described previously. In contrast to those cells migrating through the sclerotome, labelled cells on the dorsolateral pathway were not segmentally arranged along the rostrocaudal axis. DiI-labelled cells were observed in all truncal neural crest derivatives, including subepidermal presumptive pigment cells, dorsal root ganglia, and sympathetic ganglia. By varying the stage at which the injection was performed, neural crest cell emigration at the level of the wing bud was shown to occur from stage 13 through stage 22. In addition, neural crest cells were found to populate their derivatives in a ventral-to-dorsal order, with the latest emigrating cells migrating exclusively along the dorsolateral pathway.
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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.
Full textAbstract:
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. After over-expression by electroporation into the cranial neural tube and neural crest, we observed a marked redistribution of electroporated neural crest cells in the vicinity of the trigeminal ganglion. In control-electroporated embryos, numerous, labeled neural crest cells (∼80% of the population) entered the ganglion, many of which differentiated into neurons. By contrast, few (∼30% of the population) spalt-electroporated neural crest cells entered the trigeminal ganglion. Instead, they localized in the mesenchyme around the ganglionic periphery or continued further ventrally to the branchial arches. Interestingly, little or no expression of differentiation markers for neurons or other cell types was observed in spalt-electroporated neural crest cells.
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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.
Full textAbstract:
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 somites where neural crest cells do not migrate. In quail embryos, the appearance of tenascin in neural crest pathways was well correlated with the anterior-to-posterior wave of migration. The distribution of tenascin within somites was compared with that of the neural crest marker, HNK-1, in quail embryos. In the dorsal halves of quail somites which contained migrating neural crest cells, the predominant tenascin staining was in the anterior halves of the somites, codistributed with the migrating cells. In rat embryos, tenascin was detectable in the somites only in the anterior halves. Tenascin was not detectable in the matrix of cultured quail neural crest cells, but was in the matrix surrounding somite and notochord cells in vitro. Neural crest cells cultured on a substratum of tenascin did not spread and were rounded. We propose that tenascin is an important factor controlling neural crest morphogenesis, perhaps by modifying the interaction of neural crest cells with fibronectin.
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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.
Full textAbstract:
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, postmigratory neural crest cells that lack Sox10, suggesting a role of Sox10 in the survival of neural crest cells. This function is mediated by neuregulin, which acts as a survival signal for postmigratory neural crest cells in a Sox10-dependent manner. Furthermore, Sox10 is required for glial fate acquisition, as the surviving mutant neural crest cells are unable to adopt a glial fate when challenged with different gliogenic conditions. In Sox10 heterozygous mutant neural crest cells, survival appears to be normal, while fate specifications are drastically affected. Thereby, the fate chosen by a mutant neural crest cell is context dependent. Our data indicate that combinatorial signaling by Sox10, extracellular factors such as neuregulin 1, and local cell-cell interactions is involved in fine-tuning lineage decisions by neural crest stem cells. Failures in fate decision processes might thus contribute to the etiology of Waardenburg/Hirschsprung disease.
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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.
Full textAbstract:
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 identified by their epithelial morphology and immunocytochemically. As early as 1 to 2 days in culture, approximately one third of the neural crest cells stained with m217c, a monoclonal antibody that appears to recognize the same antigen as rat neural antigen-1 (RAN-1). A similar proportion of cells were immunoreactive in cultures stained with 192-IgG, a monoclonal antibody that recognizes the rat nerve growth factor receptor. The number of immunoreactive cells increased with time in culture. After 16 days in culture, nests of cells, many of which had a bipolar morphology, were present in the area previously occupied by neural crest cells. The cells in the nests were often associated with neurons and were immunoreactive for m217c, 192-IgG and antibody to S-100 protein and laminin, indicating that the cells were Schwann cells. At all culture periods examined, neural crest cells did not express glial fibrillary acidic protein. These results demonstrate that cultured premigratory neural crest cells express early Schwann cell markers and that some of these cells differentiate into Schwann cells. These observations suggest that some neural crest cells in vivo may be committed to forming Schwann cells and will do so provided that they then proceed to encounter the correct environmental cues during embryonic development.
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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.
Full textAbstract:
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 in combination with in vitro whole embryo culture to map the patterns of cranial neural crest cell migration into the developing branchial arches. Our results show that mouse hindbrain-derived neural crest cells migrate in three segregated streams adjacent to the even-numbered rhombomeres into the branchial arches, and each stream contains contributions of cells from three rhombomeres in a pattern very similar to that observed in the chick embryo. There are clear neural crest-free zones adjacent to r3 and r5. Furthermore, using grafting and lineage-tracing techniques in cultured mouse embryos to investigate the differential ability of odd and even-numbered segments to generate neural crest cells, we find that odd and even segments have an intrinsic ability to produce equivalent numbers of neural crest cells. This implies that inter-rhombomeric signalling is less important than combinatorial interactions between the hindbrain and the adjacent arch environment in specific regions, in the process of restricting the generation and migration of neural crest cells. This creates crest-free territories and suggests that tissue interactions established during development and patterning of the branchial arches may set up signals that the neural plate is primed to interpret during the progressive events leading to the delamination and migration of neural crest cells. Using interspecies grafting experiments between mouse and chick embryos, we have shown that this process forms part of a conserved mechanism for generating neural crest-free zones and contributing to the separation of migrating crest populations with distinct Hox expression during vertebrate head development.
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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.
Full textAbstract:
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/epidermal confrontations are performed in tissue culture to look at the formation of neural crest derivatives, juxtaposition of epidermis with either early (stages 4–5) or later (stages 6–10) neural plate results in the generation of both melanocytes and sympathoadrenal cells. Interestingly, neural plates isolated from early stages form no neural crest cells, whereas those isolated later give rise to melanocytes but not crest-derived sympathoadrenal cells. Single cell lineage analysis was performed to determine the time at which the neural crest lineage diverges from the epidermal lineage and to elucidate the timing of neural plate/epidermis interactions during normal development. Our results from stage 8 to 10+ embryos show that the neural plate/neural crest lineage segregates from the epidermis around the time of neural tube closure, suggesting that neural induction is still underway at open neural plate stages.
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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 mutant phenotype indicates that nrd is required for a primary wave of neural crest cell formation during which progenitors generate both RB sensory neurons and neural crest cells. Moreover, the early deficit in neural crest cells in nrd homozygotes is compensated later in development. Thus, we propose that a later wave can compensate for the loss of early neural crest cells but, interestingly, not the RB sensory neurons. We discuss the implications of these findings for the possibility that RB sensory neurons and neural crest cells share a common evolutionary origin.
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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 antigen is detectable in embryonic tissue sections on the surface of the myotome, neural tube, and notochord. The effects of the JG22 on neural crest migration in vivo were examined by a new perturbation approach in which both the antibody and the hybridoma cells were microinjected onto neural crest pathways. Hybridoma cells were labeled with a fluorescent cell marker that is nondeleterious and that is preserved after fixation and tissue sectioning. The JG22 antibody and hybridoma cells caused a marked reduction in cranial neural crest migration, a build-up of neural crest cells within the lumen of the neural tube, and some migration along aberrant pathways. Neural crest migration in the trunk was affected to a much lesser extent. In both cranial and trunk regions, a cell free zone of one or more cell diameters was generally observed between neural crest cells and the JG22 hybridoma cells. Two other monoclonal antibodies, 1-B and 1-N, were used as controls. Both 1-B and 1-N bind to bands of the 140-kD complex precipitated by JG22. Neither control antibody affected neural crest adhesion in vitro or neural crest migration in situ. This suggests that the observed alterations in neural crest migration are due to a functional block of the 140-kD complex.
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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.
Full textAbstract:
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 that neural crest regeneration occurs only after apposition of the remaining neuroepithelium with the epidermis, suggesting that the developmental mechanism underlying regeneration of the neural crest may recapitulate initial generation of the neural crest. The regulative response occurs maximally at the 3–5 somite stage, and slowly declines thereafter. Surprisingly, there are profound regional differences in the regenerative ability. Whereas a robust regulation occurs in the caudal midbrain/hindbrain, the caudal forebrain/rostral midbrain regenerates neural crest to a much lesser extent. After neural fold removal in the hindbrain, regenerated neural crest cells migrate in a segmental pattern analogous to that seen in unablated embryos; a decrease in regulative response appears to occur with increasing depth of the ablation. Up-regulation of Slug appears to be an early response after ablation, with Slug transcripts detectable proximal to the ablated region 5–8 hours after surgery and prior to emergence of neural crest cells. Both bilateral and unilateral ablations yield substantial numbers of neural crest cells, though the former recover less rapidly and have greater deficits in neural crest-derived structures than the latter. These experiments demonstrate that the regulative ability of the cranial neuroepithelium to form neural crest depends on the time, location and extent of neural fold ablation.
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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 which neural crest cells adhere tenaciously in culture. The pattern of migration through the somite may be accounted for in part by the precocious development of the basal lamina of the dermamyotome in the anterior half of the somite; this basal lamina contains both fibronectin and laminin and the neural crest cells prefer to migrate on it. In contrast, the regions into which the crest cells do not invade are filled with relatively nonadhesive molecules such as chondroitin sulphate. Some of the pathways are filled with hyaluronic acid, which stimulates the migration of neural crest cells when they are cultured in three-dimensional gels, presumably by opening spaces. Neural crest cells are also constrained to stay within the pathways by basal laminae, which act as barriers and through which crest cells do not go. Therefore, crest pathways are probably defined by several redundant factors. The directionality of crest cell migration is probably due to contact inhibition, which can be demonstrated in tissue culture. Various grafting experiments have suggested that chemotaxis and haptotaxis do not play a role in controlling the dispersion of the crest cells away from the neural tube. We have documented the extraordinary ability of neural crest cells to disperse in the embryo, even when they are grafted into sites in which they would normally not migrate. We have evidence that the cells' production of plasminogen activator, a proteolytic enzyme, and also the minimal tractional force that crest cells exert on the substratum as they migrate, contribute to this migratory ability.
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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.
Full textAbstract:
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 repeatedly imaged using low-light-level epifluorescence microscopy, permitting their movement to be followed in living embryos over time. These intravital images definitively show that neural crest cells move both rostrally and caudally from r3 and r5 to emerge as a part of the streams adjacent to r2, r4, and/or r6. Within the first few hours, cells labeled in r3 move within and/or along the dorsal neural tube surface, either rostrally toward the r2/3 border or caudally toward the r3/4 border. The labeled cells exit the surface of the neural tube near these borders and migrate toward the first or second branchial arches several hours after initial labeling. Focal DiI injections into r5 resulted in neural crest cell contributions to both the second and third branchial arches, again via rostrocaudal movements of the cells before migration into the periphery. These results demonstrate conclusively that all rhombomeres give rise to neural crest cells, and that rostrocaudal rearrangement of the cells contributes to the segmental migration of neural crest cells adjacent to r2, r4, and r6. Furthermore, it appears that there are consistent exit points of neural crest cell emigration; for example, cells arising from r3 emigrate almost exclusively from the rostral or caudal borders of that rhombomere.
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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.
Full textAbstract:
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 manner, with 0.1 and 1 ng/ml causing enhanced proliferation, and 10 ng/ml inducing cartilage differentiation. In longer-term cultures, both endochondral and membrane bone are formed. FGFR1, FGFR2 and FGFR3 are all detectable by immunohistochemistry in the mesencephalic region, with particularly intense expression at the apices of the neural folds from which the neural crest arises. FGFRs are also expressed by subpopulations of neural crest cells in culture. Collectively, these findings suggest that FGFs are involved in the skeletogenic differentiation of the cranial neural crest.
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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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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, microphthalmia and coloboma are common phenotypes in human disease and animal models in which neural crest cell specification and early migration are disrupted. In addition, neural crest cells directly contribute to numerous ocular structures including the cornea, iris, sclera, ciliary body, trabecular meshwork, and aqueous outflow tracts. Defects in later neural crest cell migration and differentiation cause a constellation of well-recognized ocular anterior segment anomalies such as Axenfeld–Rieger Syndrome and Peters Anomaly. This review will focus on the genetics of the neural crest cells within the context of how these complex processes specifically affect overall ocular development and can lead to congenital eye diseases.
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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 observations suggest that dye coupling may not be a good measure of gap junction communication relevant to motility. Alternatively, Cx43α1 may serve a novel function in motility. We observed that p120 catenin (p120ctn), an Armadillo protein known to modulate cell motility, is colocalized not only with N-cadherin but also with Cx43α1. Moreover, the subcellular distribution of p120ctn was altered with N-cadherin or Cx43α1 deficiency. Based on these findings, we propose a model in which Cx43α1 and N-cadherin may modulate neural crest cell motility by engaging in a dynamic cross-talk with the cell's locomotory apparatus through p120ctn signaling.
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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. Misexpression of FoxD3 by electroporation in the lateral neural epithelium early in neural crest development produced an expansion of HNK1 immunoreactivity throughout the neural epithelium, although these cells did not undergo an epithelial/mesenchymal transformation. To test whether FoxD3 represses melanogenesis in early migrating neural crest cells, we knocked down expression in cultured neural crest with antisense oligonucleotides and in vivo by treatment with morpholino antisense oligonucleotides. Both experimental approaches resulted in an expansion of the melanoblast lineage, probably at the expense of neuronal and glial lineages. Conversely, persistent expression of FoxD3 in late-migrating neural crest cells using RCAS viruses resulted in the failure of melanoblasts to develop. We suggest that FoxD3 plays two important roles in neural crest development. First, it is involved in the segregation of the neural crest lineage from the neuroepithelium. Second, it represses melanogenesis, thereby allowing other neural crest derivatives to differentiate during the early stages of neural crest patterning.
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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.
Full textAbstract:
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 region, we have challenged the fate of these populations by ablating the neural crest either alone or in combination with the adjoining ventral portions of the neural tube. Focal injections of the vital dye, DiI, into the neural tissue bordering the ablated region demonstrate that cells at the same axial level, in the lateral and ventral neural tube, regulate to reconstitute a population of neural crest cells. These cells emigrate from the neural tube, migrate along normal pathways according to their axial level of origin and appear to give rise to a normal range of derivatives. This regulation following ablation suggests that neural tube cells normally destined to form CNS derivatives can adjust their prospective fates to form PNS and other neural crest derivatives until 4.5-6 hours after the time of normal onset of emigration from the neural tube.
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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.
Full textAbstract:
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 crest and its derivatives in the avian embryo. Prior to emigration, neural crest cells exhibited both vinculin and talin at levels similar to the neighbouring neural epithelial cells, and this expression apparently did not change as cells became endowed with migratory properties. However, vinculin became selectively enhanced in neural crest cells as they further migrated towards their final destination. This increase in vinculin amount was particularly striking in vagal and truncal neural crest cells entering cellular environments, such as the sclerotome and the gut mesenchyme. Talin was also expressed by neural crest cells but, in contrast to vinculin, staining was not conspicuous compared to neighbouring mesenchymal cells. High levels of vinculin persisted throughout embryogenesis in almost all neural derivatives of the neural crest, including the autonomous and sensory ganglia and Schwann cells along the peripheral nerves. In contrast, the non-neural derivatives of the neural crest rapidly lost their prominent vinculin staining after migration. The pattern of talin in the progeny of the neural crest was complex and varied with the cell types: for example, some cranial sensory ganglia expressed high amounts of the molecule whereas autonomic ganglia were nearly devoid of it. Our results suggest that (i) vinculin and talin may follow independent regulatory patterns within the same cell population, (ii) the level of expression of vinculin and talin in neural crest cells may be consistent with the rapid, constant modulations of their adhesive properties, and (iii) the expression patterns of the two molecules may also be correlated with the genesis of the peripheral nervous system.
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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.
Full textAbstract:
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 their early stage of detachment from the neural crest.Hamburger and Hamilton (1951) stages 9 to 12 White Leghorn chick embryos. Fixation in 2.5% glutaraldehyde - 0.5% tanic acid and postfixation in 1% osmium tetroxide. Embryos contrasted in bloc using uranyl acetate and embedded in araldite. Semithin transversal sections stained with toluidine blue for light microscopy. Ultrathin sections contrasted with lead citrate.
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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.
Full textAbstract:
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 prelabeling with DiI or by poststaining with the HNK-1 antibody, migrate in the somites of the explants in their typical segmental pattern. Furthermore, this paradigm allows us to follow trunk neural crest migration in situ for the first time using low-light-level videomicroscopy. The trajectories of individual neural crest cells were often complex, with cells migrating in an episodic mode encompassing forward, backward and lateral movements. Frequently, neural crest cells migrated in close-knit groups of 2–4 cells, moving at mean rates of migration of 10–14 microns/hour. Treatment of the explants with the lectin peanut agglutinin (PNA) both slowed the rate and altered the pattern of neural crest migration. Neural crest cells entered both the rostral and caudal halves of the sclerotome with mean rates of migration ranging from 6 to 13 microns/hour. These results suggest that peanut agglutinin-binding molecules are required for the segmental patterning of trunk neural crest migration. Because this approach permits neural crest migration to be both observed and perturbed, it offers the promise of more direct assays of the factors that influence neural crest development.
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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.
Full textAbstract:
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 the msx family of homeobox genes with msx-2 expression preceding apoptosis in a precisely colocalised pattern. In vitro and in ovo experiments have revealed that r3 and r5 are depleted of neural crest cells by an interaction within the neural epithelium: if isolated or distanced from their normal juxtaposition with even-numbered rhombomeres, both r3 and r5 produce migrating neural crest cells. When r3 or r5 are unconstrained in this way, allowing production of crest, msx-2 expression is concomitantly down regulated. This suggests a correlation between msx-2 and the programming of apoptosis in this system. The hindbrain neural crest is thus produced in discrete streams by mechanisms intrinsic to the neural epithelium. The crest cells that enter the underlying branchial region are organised into streams before they encounter the mesodermal environment lateral to the neural tube. This contrasts sharply with the situation in the trunk where neural crest production is uninterrupted along the neuraxis and the segmental accumulation of neurogenic crest cells is subsequently founded on an alternation of permissive and non-permissive qualities of the local mesodermal environment.
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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.
Full textAbstract:
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 compared with those obtained by misdirecting neural crest cells via rhombomere rotation. Following surgical ablation of dorsal r5 and r6 prior to the 10 somite stage, r4 neural crest cells migrate along normal pathways toward the second branchial arch. Similarly, r7 neural crest cells migrate primarily to the fourth branchial arch. When analogous ablations are performed at the 10–12 somite stage, however, a marked increase in the numbers of DiI/Hoxa-3-positive cells from r7 are observed within the third branchial arch. In addition, some DiI-labeled r4 cells migrate into the depleted hindbrain region and the third branchial arch. During their migration, a subset of these r4 cells up-regulate Hoxa-3, a transcript they do not normally express. Krox20 transcript levels were augmented after ablation in a population of neural crest cells migrating from r4, caudal r3 and rostral r3. Long-term survivors of bilateral ablations possess normal neural crest-derived cartilage of the hyoid complex, suggesting that misrouted r4 and r7 cells contribute to cranial derivatives appropriate for their new location. In contrast, misdirecting of the neural crest by rostrocaudal rotation of r4 through r6 results in a reduction of Hoxa-3 expression in the third branchial arch and corresponding deficits in third arch-derived structures of the hyoid apparatus. These results demonstrate that neural crest/tube progenitors in the hindbrain can compensate by altering migratory trajectories and patterns of gene expression when the adjacent neural crest is removed, but fail to compensate appropriately when the existing neural crest is misrouted by neural tube rotation.
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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.
Full textAbstract:
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 marking experiments reveal that neural crest cells migrating caudally, but not rostrally, from r5 and caudally from r6 express Hoxa3 in normal embryo. Results from transposition experiments demonstrate that expression of Hoxa3 in r5 neural crest cells is not strictly cell-autonomous. When r5 is transposed with r4 by rostrocaudal rotation of the rhomobomeres, Hoxa3 is expressed in cells migrating lateral to transposed r5 and for a short time, in condensing ganglia, but not by neural crest within the second branchial arch. Since DiI-labeled cells from transposed r5 are present in the second arch, Hoxa3-expressing neural crest cells from r5 appear to down-regulate their Hoxa3 expression in their new environment. In contrast, when r6 is transposed to the position of r4 after boundary formation, Hoxa3 is maintained in both migrating neural crest cells and those positioned within the second branchial arch and associated ganglia. These results suggest that Hoxa3 expression is cell-autonomous in r6 and its associated neural crest. Our results suggest that neural crest cells expressing the same Hox gene are not eqivalent; they respond differently to environmental signals and exhibit distinct degrees of cell autonomy depending upon their rhombomere of origin.