Effect of oxygen concentration on morphogenesis of cranial neural folds and neural crest in cultured rat embryos

Development ◽  
1979 ◽  
Vol 54 (1) ◽  
pp. 17-35
Author(s):  
Gillian M. Morriss ◽  
D. A. T. New
Keyword(s):  
Neural Crest ◽  
Neural Crest Cell ◽  
Tube Formation ◽  
Rat Embryos ◽  
Cellular Changes ◽  
Microfilament Bundles ◽  
Neural Crest Cell Migration ◽  
High O2 ◽  
Effect Of Oxygen

Rat embryos, 9½ days old, cultured with a 5% or 10% O2 gas phase underwent normal or near-normal cranial neurulation; however, culture at 20% or 40% O2 resulted in abnormal morphogenesis of the cranial neural folds from the 9-somite stage onwards, and the brain tube frequently failed to close. Normal morphogenesis was characterized by a narrowing V-shaped profile, development of a slightly concave neuroepithelial surface, and formation of a sharp mediad curvature of the most lateral region prior to midline apposition and fusion. These morphogenetic events were related to cellular changes within the neuroepithelium, namely cell death, onset of neural crest cell migration, and loss of apical microfilament bundles from the most lateral cells. In 20% and 40% O2-cultured embryos, failure of curvature of the neuroepithelium was associated with failure or retardation of the related cellular changes; it may therefore have been due to the maintenance of an excessive rigidity which opposed the forces involved in bringing about the final stage of brain-tube formation. Mitochondria in normal (low O2 and in vivo) embryos were of the anaerobic type, having few cristae; in high O2,-cultured embryos they were of the characteristic aerobic type, indicating an adaptation to the abnormal environment.

scholarly journals Cell surface beta 1,4-galactosyltransferase functions during neural crest cell migration and neurulation in vivo

1992 ◽  
Vol 117 (2) ◽  
pp. 369-382 ◽  
Author(s):  
HJ Hathaway ◽  
BD Shur
Keyword(s):  
Cell Migration ◽  
Cell Surface ◽  
Neural Crest ◽  
Basal Lamina ◽  
Neural Tube ◽  
Neural Crest Cell ◽  
Cranial Neural Crest Cell ◽  
Neural Crest Cell Migration ◽  
Crest Cell

Mesenchymal cell migration and neurite outgrowth are mediated in part by binding of cell surface beta 1,4-galactosyltransferase (GalTase) to N-linked oligosaccharides within the E8 domain of laminin. In this study, we determined whether cell surface GalTase functions during neural crest cell migration and neural development in vivo using antibodies raised against affinity-purified chicken serum GalTase. The antibodies specifically recognized two embryonic proteins of 77 and 67 kD, both of which express GalTase activity. The antibodies also immunoprecipitated and inhibited chick embryo GalTase activity, and inhibited neural crest cell migration on laminin matrices in vitro. Anti-GalTase antibodies were microinjected into the head mesenchyme of stage 7-9 chick embryos or cranial to Henson's node of stage 6 embryos. Anti-avian GalTase IgG decreased cranial neural crest cell migration on the injected side but did not cross the embryonic midline and did not affect neural crest cell migration on the uninjected side. Anti-avian GalTase Fab crossed the embryonic midline and perturbed cranial neural crest cell migration throughout the head. Neural fold elevation and neural tube closure were also disrupted by Fab fragments. Cell surface GalTase was localized to migrating neural crest cells and to the basal surfaces of neural epithelia by indirect immunofluorescence, whereas GalTase was undetectable on neural crest cells prior to migration. These results suggest that, during early embryogenesis, cell surface GalTase participates during neural crest cell migration, perhaps by interacting with laminin, a major component of the basal lamina. Cell surface GalTase also appears to play a role in neural tube formation, possibly by mediating neural epithelial adhesion to the underlying basal lamina.

scholarly journals The distribution of tenascin coincides with pathways of neural crest cell migration

Development ◽  
1988 ◽  
Vol 102 (1) ◽  
pp. 237-250 ◽  
Author(s):  
E.J. Mackie ◽  
R.P. Tucker ◽  
W. Halfter ◽  
R. Chiquet-Ehrismann ◽  
H.H. Epperlein
Keyword(s):  
Xenopus Laevis ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Rat Embryos ◽  
The Matrix ◽  
Neural Crest Cell Migration ◽  
Neural Crest Migration ◽  
Migration Pathways

The distribution of the extracellular matrix (ECM) glycoprotein, tenascin, has been compared with that of fibronectin in neural crest migration pathways of Xenopus laevis, quail and rat embryos. In all species studied, the distribution of tenascin, examined by immunohistochemistry, was more closely correlated with pathways of migration than that of fibronectin, which is known to be important for neural crest migration. In Xenopus laevis embryos, anti-tenascin stained the dorsal fin matrix and ECM along the ventral route of migration, but not the ECM found laterally between the ectoderma and somites where neural crest cells do not migrate. In quail embryos, the appearance of tenascin in neural crest pathways was well correlated with the anterior-to-posterior wave of migration. The distribution of tenascin within somites was compared with that of the neural crest marker, HNK-1, in quail embryos. In the dorsal halves of quail somites which contained migrating neural crest cells, the predominant tenascin staining was in the anterior halves of the somites, codistributed with the migrating cells. In rat embryos, tenascin was detectable in the somites only in the anterior halves. Tenascin was not detectable in the matrix of cultured quail neural crest cells, but was in the matrix surrounding somite and notochord cells in vitro. Neural crest cells cultured on a substratum of tenascin did not spread and were rounded. We propose that tenascin is an important factor controlling neural crest morphogenesis, perhaps by modifying the interaction of neural crest cells with fibronectin.

scholarly journals DAN (NBL1) promotes collective neural crest migration by restraining uncontrolled invasion

2017 ◽  
Vol 216 (10) ◽  
pp. 3339-3354 ◽  
Author(s):  
Rebecca McLennan ◽  
Caleb M. Bailey ◽  
Linus J. Schumacher ◽  
Jessica M. Teddy ◽  
Jason A. Morrison ◽  
...  
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Metastatic Melanoma ◽  
Neural Crest Cell ◽  
Bmp Signaling ◽  
Loss Of Function ◽  
Neural Crest Cell Migration ◽  
Crest Cell

Neural crest cells are both highly migratory and significant to vertebrate organogenesis. However, the signals that regulate neural crest cell migration remain unclear. In this study, we test the function of differential screening-selected gene aberrant in neuroblastoma (DAN), a bone morphogenetic protein (BMP) antagonist we detected by analysis of the chick cranial mesoderm. Our analysis shows that, before neural crest cell exit from the hindbrain, DAN is expressed in the mesoderm, and then it becomes absent along cell migratory pathways. Cranial neural crest and metastatic melanoma cells avoid DAN protein stripes in vitro. Addition of DAN reduces the speed of migrating cells in vivo and in vitro, respectively. In vivo loss of function of DAN results in enhanced neural crest cell migration by increasing speed and directionality. Computer model simulations support the hypothesis that DAN restrains cell migration by regulating cell speed. Collectively, our results identify DAN as a novel factor that inhibits uncontrolled neural crest and metastatic melanoma invasion and promotes collective migration in a manner consistent with the inhibition of BMP signaling.

scholarly journals Extracellular Cleavage of Cadherin-11 by ADAM Metalloproteases Is Essential for Xenopus Cranial Neural Crest Cell Migration

2009 ◽  
Vol 20 (1) ◽  
pp. 78-89 ◽  
Author(s):  
Catherine McCusker ◽  
Hélène Cousin ◽  
Russell Neuner ◽  
Dominique Alfandari
Keyword(s):  
Cell Adhesion ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Cranial Neural Crest ◽  
Downstream Signaling ◽  
Cranial Neural Crest Cell ◽  
Neural Crest Cell Migration ◽  
Membrane Bound

Cell adhesion molecules such as cadherins alternate their expression throughout cranial neural crest (CNC) development, yet our understanding of the role of these molecules during CNC migration remains incomplete. The “mesenchymal” cadherin-11 is expressed in the CNC during migration yet prevents migration when overexpressed in the embryo, suggesting that a defined level of cadherin-11–mediated cell adhesion is required for migration. Here we show that members of the meltrin subfamily of ADAM metalloproteases cleave the extracellular domain of cadherin-11 during CNC migration. We show that a fragment corresponding to the putative shed form of cadherin-11 retains biological activity by promoting CNC migration in vivo, in a non-cell–autonomous manner. Additionally, cleavage of cadherin-11 does not affect binding to β-catenin and downstream signaling events. We propose that ADAM cleavage of cadherin-11 promotes migration by modifying its ability to support cell–cell adhesion while maintaining the membrane-bound pool of β-catenin associated with the cadherin-11 cytoplasmic domain.

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