P95. BMP-switching regulates lineage specification and migration of neural crest cells
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Neural crest cells are thought to play a critical role in human conotruncal morphogenesis and dysmorphogenesis. Much of our understanding of the contribution of neural crest to cardiovascular patterning comes from ablation and transplantation experiments in avian species. Although fate mapping experiments in mice suggests a conservation of function, the functional requirement for neural crest in cardiovascular development in mammals has not been formally tested. We used a novel two component genetic system for the temporal-spatial ablation of neural crest in the mouse. Affected embryos displayed a spectrum of cardiovascular outflow tract defects and aortic arch patterning abnormalities. We show that the severity of the cardiovascular phenotype is directly related to the level and extent of neural crest ablation. This is the first report of cardiac neural crest ablation in mammals, and it provides important insight into the role of the mammalian neural crest during cardiovascular development.
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Abstract wnt11r is a recently identified member of the Wnt family of genes, which has been proposed to be the true Xenopus homologue to the mammalian wnt11 gene. In this study we have examined the role of wnt11r on neural crest development. Expression analysis of wnt11r and comparison with the neural crest marker snail2 and the noncanonical Wnt, wnt11 , shows wnt11r is expressed at the medial or neural plate side of the neural crest while wnt11 is expressed at the lateral or epidermal side. Injection of wnt11r morpholino leads to strong inhibition of neural crest migration with no effect on neural crest induction or maintenance. This effect can be rescued by co‐injection of Wnt11r but not by Wnt11 mRNA, demonstrating the specificity of the loss of function treatment. Finally, neural crest graft experiments show that wnt11r is required in a non–cell‐autonomous manner to control neural crest migration. Developmental Dynamics 237:3404–3409, 2008. © 2008 Wiley‐Liss, Inc.
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ABSTRACT A subpopulation of neural crest termed the cardiac neural crest is required in avian embryos to initiate reorganization of the outflow tract of the developing cardiovascular system. In mammalian embryos, it has not been previously experimentally possible to study the long-term fate of this population, although there is strong inference that a similar population exists and is perturbed in a number of genetic and teratogenic contexts. We have employed a two-component genetic system based on Cre/lox recombination to label indelibly the entire mouse neural crest population at the time of its formation, and to detect it at any time thereafter. Labeled cells are detected throughout gestation and in postnatal stages in major tissues that are known or predicted to be derived from neural crest. Labeling is highly specific and highly efficient. In the region of the heart, neural-crest-derived cells surround the pharyngeal arch arteries from the time of their formation and undergo an altered distribution coincident with the reorganization of these vessels. Labeled cells populate the aorticopulmonary septum and conotruncal cushions prior to and during overt septation of the outflow tract, and surround the thymus and thyroid as these organs form. Neural-crest-derived mesenchymal cells are abundantly distributed in midgestation (E9.5-12.5), and adult derivatives of the third, fourth and sixth pharyngeal arch arteries retain a substantial contribution of labeled cells. However, the population of neural-crest-derived cells that infiltrates the conotruncus and which surrounds the noncardiac pharyngeal organs is either overgrown or selectively eliminated as development proceeds, resulting for these tissues in a modest to marginal contribution in late fetal and postnatal life.
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Neural Crest Development The vertebrate neural crest is characterized by a migratory population of multipotent cells that spread out from the dorsal side of the neural tube. Many different cell types and tissues originate here, including cells of the peripheral nervous system, the adrenal medulla, melanocytes, and some skeletal cells. Dysregulation of neural crest cells can lead to defects in cell differentiation and the cell cycle, as well as to the formation of ectopic tissue, which can result in various human diseases. Takahashi et al. (p. 860 ) review the normal development of neural crest cells, highlighting important associations of this cell population with local environments to influence tissue interactions and function, and describe pathogenesis that results when developmental events go awry.
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Neural crest cells play many key roles in embryonic development, as demonstrated by the abnormalities that result from their specific absence or dysfunction. Unfortunately, these key cells are particularly sensitive to abnormalities in various intrinsic and extrinsic factors, such as genetic deletions or ethanol‐exposure that lead to morbidity and mortality for organisms. This review discusses the role identified for a segment of neural crest in regulating the morphogenesis of the heart and associated great vessels. The paradox is that their derivatives constitute a small proportion of cells to the cardiovascular system. Findings supporting that these cells impact early cardiac function raises the interesting possibility that they indirectly control cardiovascular development at least partially through regulating function. Making connections between insults to the neural crest, cardiac function, and morphogenesis is more approachable with technological advances. Expanding our understanding of early functional consequences could be useful in improving diagnosis and testing therapies. Birth Defects Research (Part C) 102:227–250, 2014. © 2014 Wiley Periodicals, Inc.
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Newborn mice were injected with measured doses of EDTA, resulting in the development of a complex of multiple neural crest tumors, hyperplasia, excessive cell proliferation, cell death of neural crest cells and heterotopic melanin pigmentation in the sites where the neural crest cells are present. The occurrence of multiple neural crest tumors as well as the mechanism of EDTA as a teratogen may be associated with cell membrane perturbation. Oncogenesis of neural crest tumors and cell death of neural crest cells from a single agent showed the complexity and variability of phenotypic expression. Neural crest cells may differentiate into many divergent cellular phenotypes derived from an initially undifferentiated stem cell population.
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