scholarly journals Critical numbers of neural crest cells are required in the pathways from the neural tube to the foregut to ensure complete enteric nervous system formation

Development ◽  
2008 ◽  
Vol 135 (9) ◽  
pp. 1681-1691 ◽  
Author(s):  
A. J. Barlow ◽  
A. S. Wallace ◽  
N. Thapar ◽  
A. J. Burns
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Enteric Nervous System ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
System Formation

scholarly journals Enteric nervous system formation: disproportionate stochastic clonal expansion of a few initiating vagal neural crest cells

2017 ◽  
Vol 145 ◽  
pp. S40-S41
Author(s):  
Donald Newgreen ◽  
Dongcheng Zhang ◽  
James Osborne ◽  
Bevan Cheeseman ◽  
Benjamin Binder ◽  
...  
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Enteric Nervous System ◽  
Neural Crest Cells ◽  
Clonal Expansion ◽  
System Formation

scholarly journals Vital dye labelling demonstrates a sacral neural crest contribution to the enteric nervous system of chick and mouse embryos

Development ◽  
1991 ◽  
Vol 111 (4) ◽  
pp. 857-866 ◽  
Author(s):  
G.N. Serbedzija ◽  
S. Burgan ◽  
S.E. Fraser ◽  
M. Bronner-Fraser
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Enteric Nervous System ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Mouse Embryos ◽  
Chick Embryos ◽  
Vital Dye ◽  
Dorsal Portion ◽  
Sacral Neural Crest

We have used the vital dye, DiI, to analyze the contribution of sacral neural crest cells to the enteric nervous system in chick and mouse embryos. In order to label premigratory sacral neural crest cells selectively, DiI was injected into the lumen of the neural tube at the level of the hindlimb. In chick embryos, DiI injections made prior to stage 19 resulted in labelled cells in the gut, which had emerged from the neural tube adjacent to somites 29–37. In mouse embryos, neural crest cells emigrated from the sacral neural tube between E9 and E9.5. In both chick and mouse embryos, DiI-labelled cells were observed in the rostral half of the somitic sclerotome, around the dorsal aorta, in the mesentery surrounding the gut, as well as within the epithelium of the gut. Mouse embryos, however, contained consistently fewer labelled cells than chick embryos. DiI-labelled cells first were observed in the rostral and dorsal portion of the gut. Paralleling the maturation of the embryo, there was a rostral-to-caudal sequence in which neural crest cells populated the gut at the sacral level. In addition, neural crest cells appeared within the gut in a dorsal-to-ventral sequence, suggesting that the cells entered the gut dorsally and moved progressively ventrally. The present results resolve a long-standing discrepancy in the literature by demonstrating that sacral neural crest cells in both the chick and mouse contribute to the enteric nervous system in the postumbilical gut.

Zebrafishcolourlessencodessox10and specifies non-ectomesenchymal neural crest fates

Development ◽  
2001 ◽  
Vol 128 (21) ◽  
pp. 4113-4125 ◽  
Author(s):  
Kirsten A. Dutton ◽  
Angela Pauliny ◽  
Susana S. Lopes ◽  
Stone Elworthy ◽  
Tom J. Carney ◽  
...  
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Enteric Nervous System ◽  
Pigment Cell ◽  
Neural Crest Cells ◽  
Cell Number ◽  
Primary Role ◽  
Biological Basis ◽  
Sox10 Expression ◽  
Mitf Expression

Waardenburg-Shah syndrome combines the reduced enteric nervous system characteristic of Hirschsprung’s disease with reduced pigment cell number, although the cell biological basis of the disease is unclear. We have analysed a zebrafish Waardenburg-Shah syndrome model. We show that the colourless gene encodes a sox10 homologue, identify sox10 lesions in mutant alleles and rescue the mutant phenotype by ectopic sox10 expression. Using iontophoretic labelling of neural crest cells, we demonstrate that colourless mutant neural crest cells form ectomesenchymal fates. By contrast, neural crest cells which in wild types form non-ectomesenchymal fates generally fail to migrate and do not overtly differentiate. These cells die by apoptosis between 35 and 45 hours post fertilisation. We provide evidence that melanophore defects in colourless mutants can be largely explained by disruption of nacre/mitf expression. We propose that all defects of affected crest derivatives are consistent with a primary role for colourless/sox10 in specification of non-ectomesenchymal crest derivatives. This suggests a novel mechanism for the aetiology of Waardenburg-Shah syndrome in which affected neural crest derivatives fail to be generated from the neural crest.

Characterization of HNK-1 antigens during the formation of the avian enteric nervous system

Development ◽  
1992 ◽  
Vol 115 (2) ◽  
pp. 561-572 ◽  
Author(s):  
T.M. Luider ◽  
M.J. Peters-van der Sanden ◽  
J.C. Molenaar ◽  
D. Tibboel ◽  
A.W. van der Kamp ◽  
...  
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Enteric Nervous System ◽  
Plasma Membranes ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Mesenchymal Cells ◽  
Membrane Glycoproteins ◽  
Cell Colonization ◽  
Crest Cell

During vertebrate embryogenesis, interaction between neural crest cells and the enteric mesenchyme gives rise to the development of the enteric nervous system. In birds, monoclonal antibody HNK-1 is a marker for neural crest cells from the entire rostrocaudal axis. In this study, we aimed to characterize the HNK-1 carrying cells and antigen(s) during the formation of the enteric nervous system in the hindgut. Immunohistological findings showed that HNK-1-positive mesenchymal cells are present in the gut prior to neural crest cell colonization. After neural crest cell colonization this cell type cannot be visualized anymore with the HNK-1 antibody. We characterized the HNK-1 antigens that are present before and after neural crest cell colonization of the hindgut. Immunoblot analysis of plasma membranes from embryonic hindgut revealed a wide array of HNK-1-carrying glycoproteins. We found that two HNK-1 antigens are present in E4 hindgut prior to neural crest cell colonization and that the expression of these antigens disappears after neural crest colonization. These two membrane glycoproteins, G-42 and G-44, have relative molecular masses of 42,000 and 44,000, respectively, and they both have isoelectric points of 5.5 under reducing conditions. We suggest that these HNK-1 antigens and the HNK-1-positive mesenchymal cells have some role in the formation of the enteric nervous system.

scholarly journals Neural crest regionalisation for enteric nervous system formation: Implications for Hirschsprung's disease and stem cell therapy

2010 ◽  
Vol 339 (2) ◽  
pp. 280-294 ◽  
Author(s):  
Dongcheng Zhang ◽  
Inigo M. Brinas ◽  
Benjamin J. Binder ◽  
Kerry A. Landman ◽  
Donald F. Newgreen
Keyword(s):  
Nervous System ◽  
Stem Cell ◽  
Cell Therapy ◽  
Neural Crest ◽  
Enteric Nervous System ◽  
Stem Cell Therapy ◽  
Hirschsprung's Disease ◽  
Hirschsprung’S Disease ◽  
System Formation

scholarly journals A neural crest cell isotropic-to-nematic phase transition in the developing mammalian gut

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Nicolas R. Chevalier ◽  
Yanis Ammouche ◽  
Anthony Gomis ◽  
Lucas Langlois ◽  
Thomas Guilbert ◽  
...  
Keyword(s):  
Phase Transition ◽  
Extracellular Matrix ◽  
Nervous System ◽  
Smooth Muscle ◽  
Neural Crest ◽  
Enteric Nervous System ◽  
Nematic Phase ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Crest Cell

AbstractWhile the colonization of the embryonic gut by neural crest cells has been the subject of intense scrutiny over the past decades, we are only starting to grasp the morphogenetic transformations of the enteric nervous system happening in the fetal stage. Here, we show that enteric neural crest cell transit during fetal development from an isotropic cell network to a square grid comprised of circumferentially-oriented cell bodies and longitudinally-extending interganglionic fibers. We present ex-vivo dynamic time-lapse imaging of this isotropic-to-nematic phase transition and show that it occurs concomitantly with circular smooth muscle differentiation in all regions of the gastrointestinal tract. Using conditional mutant embryos with enteric neural crest cells depleted of β1-integrins, we show that cell-extracellular matrix anchorage is necessary for ganglia to properly reorient. We demonstrate by whole mount second harmonic generation imaging that fibrous, circularly-spun collagen I fibers are in direct contact with neural crest cells during the orientation transition, providing an ideal orientation template. We conclude that smooth-muscle associated extracellular matrix drives a critical reorientation transition of the enteric nervous system in the mammalian fetus.

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