In Vitro Analysis of Quail Neural Crest Cell Differentiation

1985 ◽  
pp. 193-222 ◽  
Author(s):  
Maya Sieber-Blum ◽  
Fritz Sieber
1981 ◽  
Vol 82 (1) ◽  
pp. 86-94 ◽  
Author(s):  
Jeanne Loring ◽  
Bengt Glimelius ◽  
Carol Erickson ◽  
James A. Weston

Development ◽  
1996 ◽  
Vol 122 (3) ◽  
pp. 823-830 ◽  
Author(s):  
M. Kanatsu ◽  
S.I. Nishikawa

In murine embryogenesis, all cells that will constitute the embryonic structures originate from the epiblast (primitive ectoderm) tissue, the epithelial cell sheet of the gastrulating embryo. The cells of this tissue are totipotent at the beginning of gastrulation, but at the end of this period are specified to particular cell lineages. Thus, it is likely that during murine gastrulation, the potency of epiblast cells that were originally totipotent becomes restricted as development progresses. However, the mechanisms of this process are unknown. We have investigated this process in vitro, focusing on the hematopoietic cell lineage. To detect the hematogenic potency of the epiblast tissue, we established an in vitro culture system in which the hematopoietic cell differentiation of the epiblast tissue was supported by a stromal cell layer. With this culture system, we investigated the process by which this potency becomes spatially and temporally restricted during gastrulation. The results showed that hematogenic potency resides in the entire epiblast of the early- to mid-gastrulating embryo, but becomes restricted to the posterior half of the epiblast at the headfold stage. Furthermore, we showed that this process is altered by exogenous bone morphogenetic protein-4 (BMP-4) or activin A, which may be mesoderm inducers in Xenopus embryogenesis.


2018 ◽  
Vol 11 (12) ◽  
pp. dmm035097 ◽  
Author(s):  
Maria R. Replogle ◽  
Virinchipuram S. Sreevidya ◽  
Vivian M. Lee ◽  
Michael D. Laiosa ◽  
Kurt R. Svoboda ◽  
...  

2013 ◽  
Vol 5 (2) ◽  
pp. a008326-a008326 ◽  
Author(s):  
S. Bhatt ◽  
R. Diaz ◽  
P. A. Trainor

Development ◽  
1999 ◽  
Vol 126 (10) ◽  
pp. 2181-2189 ◽  
Author(s):  
B.J. Eickholt ◽  
S.L. Mackenzie ◽  
A. Graham ◽  
F.S. Walsh ◽  
P. Doherty

Collapsin-1 belongs to the Semaphorin family of molecules, several members of which have been implicated in the co-ordination of axon growth and guidance. Collapsin-1 can function as a selective chemorepellent for sensory neurons, however, its early expression within the somites and the cranial neural tube (Shepherd, I., Luo, Y., Raper, J. A. and Chang, S. (1996) Dev. Biol. 173, 185–199) suggest that it might contribute to the control of additional developmental processes in the chick. We now report a detailed study on the expression of collapsin-1 as well as on the distribution of collapsin-1-binding sites in regions where neural crest cell migration occurs. collapsin-1 expression is detected in regions bordering neural crest migration pathways in both the trunk and hindbrain regions and a receptor for collapsin-1, neuropilin-1, is expressed by migrating crest cells derived from both regions. When added to crest cells in vitro, a collapsin-1-Fc chimeric protein induces morphological changes similar to those seen in neuronal growth cones. In order to test the function of collapsin-1 on the migration of neural crest cells, an in vitro assay was used in which collapsin-1-Fc was immobilised in alternating stripes consisting of collapsin-Fc/fibronectin versus fibronectin alone. Explanted neural crest cells derived from both trunk and hindbrain regions avoided the collapsin-Fc-containing substratum. These results suggest that collapsin-1 signalling can contribute to the patterning of neural crest cell migration in the developing chick.


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