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Crest Cell Migration (crest + cell_migration)

Distribution by Scientific Domains
Life Sciences87%

Kinds of Crest Cell Migration

  • neural crest cell migration
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    Selected Abstracts

    Regulation of the Neurofibromatosis 2 gene promoter expression during embryonic development

    DEVELOPMENTAL DYNAMICS, Issue 10 2006
    Elena M. Akhmametyeva
    Abstract Mutations in the Neurofibromatosis 2 (NF2) gene are associated with predisposition to vestibular schwannomas, spinal schwannomas, meningiomas, and ependymomas. Presently, how NF2 is expressed during embryonic development and in the tissues affected by neurofibromatosis type 2 (NF2) has not been well defined. To examine NF2 expression in vivo, we generated transgenic mice carrying a 2.4-kb NF2 promoter driving ,-galactosidase (,-gal) with a nuclear localization signal. Whole-mount embryo staining revealed that the NF2 promoter directed ,-gal expression as early as embryonic day E5.5. Strong expression was detected at E6.5 in the embryonic ectoderm containing many mitotic cells. ,-gal staining was also found in parts of embryonic endoderm and mesoderm. The ,-gal staining pattern in the embryonic tissues was corroborated by in situ hybridization analysis of endogenous Nf2 RNA expression. Importantly, we observed strong NF2 promoter activity in the developing brain and in sites containing migrating cells including the neural tube closure, branchial arches, dorsal aorta, and paraaortic splanchnopleura. Furthermore, we noted a transient change of NF2 promoter activity during neural crest cell migration. While little ,-gal activity was detected in premigratory neural crest cells at the dorsal ridge region of the neural fold, significant activity was seen in the neural crest cells already migrating away from the dorsal neural tube. In addition, we detected considerable NF2 promoter activity in various NF2-affected tissues such as acoustic ganglion, trigeminal ganglion, spinal ganglia, optic chiasma, the ependymal cell-containing tela choroidea, and the pigmented epithelium of the retina. The NF2 promoter expression pattern during embryogenesis suggests a specific regulation of the NF2 gene during neural crest cell migration and further supports the role of merlin in cell adhesion, motility, and proliferation during development. Developmental Dynamics 235:2771,2785, 2006. © 2006 Wiley-Liss, Inc. [source]

    Tissue inhibitor of metalloproteinase-2 (TIMP-2) expression during cardiac neural crest cell migration and its role in proMMP-2 activation

    DEVELOPMENTAL DYNAMICS, Issue 4 2004
    V. Cantemir
    Abstract Matrix metalloproteinases (MMPs) are important mediators of neural crest (NC) cell migration. Here, we examine the distribution of tissue inhibitor of metalloproteinase (TIMP) -2 and TIMP-3 and test whether manipulating TIMP levels alters chicken cardiac NC cell migration. TIMP-2 mRNA is expressed at stage 11 in the neural epithelium and only in migrating cardiac NC cells. TIMP-3 mRNA is expressed only in the notochord at stage 8 and later in the outflow tract myocardium. Exogenous TIMP-2 increases NC motility in vitro at low concentrations but has no effect when concentrations are increased. In vitro, NC cells express membrane type-1 matrix metalloproteinase (MT1-MMP) and TIMP-2 and they secrete and activate proMMP-2. Antisense TIMP-2 oligonucleotides block proMMP-2 activation, decrease NC cell migration from explants, and perturb NC morphogenesis in ovo. Because TIMP-2 is required for activation of proMMP-2 by MT1-MMP, this finding suggests TIMP-2 expression by cardiac NC cells initiates proMMP-2 activation important for their migration. Developmental Dynamics 231:709,719, 2004. © 2004 Wiley-Liss, Inc. [source]

    Early differentiation and migration of cranial neural crest in the opossum, Monodelphis domestica

    EVOLUTION AND DEVELOPMENT, Issue 2 2003
    Janet L. Vaglia
    SUMMARY Marsupial mammals are born at a highly altricial state. Nonetheless, the neonate must be capable of considerable functional independence. Comparative studies have shown that in marsupials the morphogenesis of many structures critical to independent function are advanced relative to overall development. Many skeletal and muscular elements in the facial region show particular heterochrony. Because neural crest cells are crucial to forming and patterning much of the face, this study investigates whether the timing of cranial neural crest differentiation is also advanced. Histology and scanning electron microscopy of Monodelphis domestica embryos show that many aspects of cranial neural crest differentiation and migration are conserved in marsupials. For example, as in other vertebrates, cranial neural crest differentiates at the neural ectoderm/epidermal boundary and migrates as three major streams. However, when compared with other vertebrates, a number of timing differences exist. The onset of cranial neural crest migration is early relative to both neural tube development and somite formation in Monodelphis. First arch neural crest cell migration is particularly advanced and begins before any somites appear or regional differentiation exists in the neural tube. Our study provides the first published description of cranial neural crest differentiation and migration in marsupials and offers insight into how shifts in early developmental processes can lead to morphological change. [source]

    Cranial neural crest cell migration in the Australian lungfish, Neoceratodus forsteri

    EVOLUTION AND DEVELOPMENT, Issue 4 2000
    Pierre Falck
    SUMMARY A crucial role for the cranial neural crest in head development has been established for both actinopterygian fishes and tetrapods. It has been claimed, however, that the neural crest is unimportant for head development in the Australian lungfish (Neoceratodus forsteri ,), a member of the group (Dipnoi) which is commonly considered to be the living sister group of the tetrapods. In the present study, we used scanning electron microscopy to study cranial neural crest development in the Australian lungfish. Our results, contrary to those of Kemp, show that cranial neural crest cells do emerge and migrate in the Australian lungfish in the same way as in other vertebrates, forming mandibular, hyoid, and branchial streams. The major difference is in the timing of the onset of cranial neural crest migration. It is delayed in the Australian lungfish in comparison with their living sister group the Lissamphibia. Furthermore, the delay in timing between the emergence of the hyoid and branchial crest streams is very long, indicating a steeper anterior-posterior gradient than in amphibians. We are now extending our work on lungfish head development to include experimental studies (ablation of selected streams of neural crest cells) and fate mapping (using fluoresent tracer dyes such as DiI) to document the normal fate as well as the role in head patterning of the cranial neural crest in the Australian lungfish. [source]

    Patterned assembly and neurogenesis in the chick dorsal root ganglion

    THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 4 2010
    Lynn George
    The birth of small-diameter TrkA+ neurons that mediate pain and thermoreception begins ,24 hours after the cessation of neural crest cell migration from progenitors residing in the nascent dorsal root ganglion. Although multiple geographically distinct progenitor pools have been proposed, this study is the first to comprehensively characterize the derivation of small-diameter neurons. In the developing chick embryo we identify novel patterns in neural crest cell migration and colonization that sculpt the incipient ganglion into a postmitotic neuronal core encapsulated by a layer of proliferative progenitor cells. Furthermore, we show that this outer progenitor layer is composed of three spatially, temporally, and molecularly distinct progenitor zones, two of which give rise to distinct populations of TrkA+ neurons. J. Comp. Neurol. 518:405,422, 2010. © 2009 Wiley-Liss, Inc. [source]

    Patterned assembly and neurogenesis in the chick dorsal root ganglion

    THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 4 2010
    Lynn George
    Abstract The birth of small-diameter TrkA+ neurons that mediate pain and thermoreception begins ,24 hours after the cessation of neural crest cell migration from progenitors residing in the nascent dorsal root ganglion. Although multiple geographically distinct progenitor pools have been proposed, this study is the first to comprehensively characterize the derivation of small-diameter neurons. In the developing chick embryo we identify novel patterns in neural crest cell migration and colonization that sculpt the incipient ganglion into a postmitotic neuronal core encapsulated by a layer of proliferative progenitor cells. Furthermore, we show that this outer progenitor layer is composed of three spatially, temporally, and molecularly distinct progenitor zones, two of which give rise to distinct populations of TrkA+ neurons. J. Comp. Neurol. 518:405,422, 2010. © 2009 Wiley-Liss, Inc. [source]

    Disturbed morphogenesis of cardiac outflow tract and increased rate of aortic arch anomalies in the offspring of diabetic rats

    BIRTH DEFECTS RESEARCH, Issue 12 2004
    Daniël G.M. Molin
    Abstract BACKGROUND Maternal diabetes (MD) is a risk factor for offspring to develop cardiovascular anomalies; this is of growing clinical concern since the number of women in childbearing age with compromised glucose homeostasis is increasing. Hyperglycemia abrogates cardiovascular development in vitro; however, a link to cardiovascular defects in diabetic offspring remains to be investigated. METHODS We have studied cardiovascular development in offspring of MD rats by examining serial histological sections of GD 12.0,18.0 offspring. Development of pharyngeal arch artery malformations was analyzed and related to intracardiac anomalies. RESULTS Pharyngeal arch artery and intracardiac defects were present in 27 of 37 MD GD 13.0,18.0 offspring. Early sixth arch arteries showed abrogated arteriogenesis, whereas fourth arch artery defects developed as a result of abnormal remodeling. Morphometrical analysis showed increased apoptosis in regressing artery segments and reduced apoptosis in persisting artery segments. Double outlet right ventricle with infundibular stenosis (tetralogy of Fallot) was predominantly found in combination with sixth artery defects and pulmonary atresia. As confirmed by morphometric analysis and three-dimensional (3D)-reconstructions, outflow tract defects coincided with endocardial cushion hypoplasia. Cases with teratology of Fallot additionally showed a shorter outflow tract. No relation with apoptosis or disturbed neural crest cell migration was found. CONCLUSIONS Our data uniquely demonstrate mechanistic differences involved in the development of sixth and fourth artery anomalies. Whereas increased apoptosis induces fourth artery anomalies, pulmonary outflow obstruction abrogates sixth artery differentiation independent of apoptosis. The model presented allows analysis of diabetic conditions on cardiovascular development in vivo, essential for elucidating this teratology. Birth Defects Research (Part A), 2004. © 2004 Wiley-Liss, Inc. [source]

    Goldenhar syndrome and neuroblastoma: a chance association?

    ACTA PAEDIATRICA, Issue 10 2003
    C Michel-Adde
    Oculoauriculovertebral dysplasia, also called Goldenhar syndrome, includes several anomalies: epibulbar dermoids or lipodermoids, microtia, mandibular hypoplasia, vertebral, skeletal, cardiac and kidney anomalies, among others. Tumours have also been observed in patients with oculoauriculovertebral dysplasia. We report the first case of oculoauriculovertebral dysplasia associated with a neuroblastoma. This tumour consists of cells identical to early migratory neural crest cells in the embryo. Several theories have been proposed regarding the pathogenetic explanation of oculoauriculovertebral dysplasia. Currently, some researchers have suggested a deficiency in mesodermal formation or defective interaction between neural crest and mesoderm as a possible aetiology. Conclusion: It is suggested that the case reported here is an additional argument for an anomaly in neural crest cell migration or interaction with the mesoderm in the pathogenesis of oculoauriculovertebral dysplasia. [source]