Neural crest cells and skeletogenesis in vertebrate embryos

1981 ◽  
Vol 13 (4) ◽  
pp. 631-642 ◽  
Author(s):  
Peter Thorogood
2018 ◽  
Author(s):  
Elsy Buitrago-Delgado ◽  
Elizabeth N. Schock ◽  
Kara Nordin ◽  
Carole LaBonne

AbstractThe neural crest is a stem cell population unique to vertebrate embryos that gives rise to derivatives from multiple embryonic germ layers. The molecular underpinnings of potency that govern neural crest potential are highly conserved with that of pluripotent blastula stem cells, suggesting that neural crest cells may have evolved through retention of aspects of the pluripotency gene regulatory network (GRN). A striking difference in the regulatory factors utilized in pluripotent blastula cells and neural crest cells is the deployment of different subfamilies of Sox transcription factors; SoxB1 factors play central roles in the pluripotency of naïve blastula and ES cells, whereas neural crest cells require SoxE function. Here we explore the shared and distinct activities of these factors to shed light on the role that this molecular hand-off of Sox factor activity plays in the genesis of neural crest and the lineages derived from it. Our findings provide evidence that SoxB1 and SoxE factors have both overlapping and distinct activities in regulating pluripotency and lineage restriction in the embryo. We hypothesize that SoxE factors may transiently replace SoxB1 factors to control pluripotency in neural crest cells, and then poise these cells to contribute to glial, chondrogenic and melanocyte lineages at stages when SoxB1 factors promote neuronal progenitor formation.


2004 ◽  
Vol 166 (5) ◽  
pp. 673-684 ◽  
Author(s):  
Ming Fu ◽  
Vincent Chi Hang Lui ◽  
Mai Har Sham ◽  
Vassilis Pachnis ◽  
Paul Kwong Hang Tam

Enteric neural crest cells (NCCs) migrate and colonize the entire gut and proliferate and differentiate into neurons and glia of the enteric nervous system in vertebrate embryos. We have investigated the mitogenic and morphogenic functions of Sonic hedgehog (Shh) on enteric NCCs in cell and organ culture. Enteric NCCs expressed Shh receptor Patched and transcripts encoding the Shh signal transducer (Gli1). Shh promoted the proliferation and inhibited the differentiation of NCCs. The pro-neurogenic effect of glial cell line–derived neurotrophic factor (GDNF) on NCCs was abolished by Shh. In gut explants, NCCs migrated from the explants onto the adjacent substratum if GDNF was added, whereas addition of Shh abolished this migration. Neuronal differentiation and coalescence of neural crest–derived cells into myenteric plexuses in explants was repressed by the addition of Shh. Our data suggest that Shh controls the proliferation and differentiation of NCCs and modulates the responsiveness of NCCs toward GDNF inductions.


Development ◽  
1998 ◽  
Vol 125 (21) ◽  
pp. 4205-4213 ◽  
Author(s):  
Y. Wakamatsu ◽  
M. Mochii ◽  
K.S. Vogel ◽  
J.A. Weston

Neural crest cells of vertebrate embryos disperse on distinct pathways and produce different derivatives in specific embryonic locations. In the trunk of avian embryos, crest-derived cells that initially migrate on the lateral pathway, between epidermal ectoderm and somite, produce melanocytes but no neuronal derivatives. Although we found that melanocyte precursors are specified before they disperse on the lateral pathway, we also observed that a few crest-derived neuronal cells are briefly present on the same pathway. Here, we show that neuronal cells are removed by an episode of apoptosis. These observations suggest that localized environmental factor(s) affect the distribution of fate-restricted crest derivatives and function as a ‘proof-reading mechanism’ to remove ‘ectopic’ crest-derived cells.


Development ◽  
1996 ◽  
Vol 122 (1) ◽  
pp. 381-389 ◽  
Author(s):  
S. Jesuthasan

Neural crest cells in the trunk of vertebrate embryos have a choice of pathways after emigrating from the neural tube: they can migrate in either the medial pathway between somites and neural tube, or the lateral pathway between somites and epidermis. In zebrafish embryos, the first cells to migrate all choose the medial pathway. High resolution imaging of cells in living embryos suggests that neural crest cells do so because of repulsion by somites: cells take the medial pathway because the lateral somite surface triggers a paralysis and retraction of protrusions (contact inhibition or collapse) when the medial surface does not. Partial deletion of somites, using the spadetail mutation allows precocious entry into the lateral pathway, but only where somites are absent, supporting the notion that an inhibitory cue on somites delays entry. Growth cones of Rohon-Beard cells enter the lateral pathway before neural crest cells, demonstrating that there is no absolute barrier to migration. These data, in addition to providing a detailed picture of neural crest cells migrating in vivo, suggest that neural crest cells, like neuronal growth cones, are guided by a specific cue that triggers ‘collapse’ of active protrusions.


2007 ◽  
Vol 27 (1) ◽  
pp. 45-52
Author(s):  
Koh-ichi Atoh ◽  
Manae S. Kurokawa ◽  
Hideshi Yoshikawa ◽  
Chieko Masuda ◽  
Erika Takada ◽  
...  

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