Growth and development of pattern in the cranial neural epithelium of rat embryos during neurulation

Development ◽  
1981 ◽  
Vol 65 (Supplement) ◽  
pp. 225-241
Author(s):  
Gillian M. Morriss-Kay
Keyword(s):  
Neural Crest ◽  
Neural Crest Cell ◽  
Cell Number ◽  
Culture Technique ◽  
Mitotic Spindles ◽  
Rat Embryos ◽  
Constant Area ◽  
High Level ◽  
Crest Cell

The pattern of growth and morphogenesis of the cranial neural epithelium of rat embryos during neurulation is described. Transverse sections of the midbrain/hindbrain neural epithelium at different stages (0–14 somites) show a constant area and cell number throughout neurulation, even though there is a high level of mitosis. Mitotic spindles are orientated parallel to the long axis of the embryo, so that increase in cell number occurs in this direction only. Growth is expressed only as an increase in size of the forebrain, which projects rostrad to the tip of the notochord. In the midbrain/upper hindbrain regions, cellular organization of the neural epithelium changes from columnar to cuboidal to pseudostratified, while its shape changes from flat to biconvex to V shaped. Closure is immediately preceded by neural crest cell emigration from the lateral edges. Throughout neurulation the cranial notochord develops an increasingly convex curvature in the rostrocaudal plane. The attached neural epithelium curves with the notochord (forming the primary cranial flexure) so that as its lateral edges move dorsomedially they form a more distant concentric arc with that of the notochord, and are hence stretched during the final closure period. The whole rat embryo culture technique was used to investigate the morphogenetic role of proteoglycans during neurulation, neural crest cell emigration and other events in the lateral edge region prior to closure, and the importance of microfilament contraction during concave curvature of the neural epithelium.

scholarly journals Role of FGF signalling in neural crest cell migration during early chick embryo development

Zygote ◽  
2018 ◽  
Vol 26 (6) ◽  
pp. 457-464 ◽  
Author(s):  
Xiao-tan Zhang ◽  
Guang Wang ◽  
Yan Li ◽  
Manli Chuai ◽  
Kenneth Ka Ho Lee ◽  
...  
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Neural Crest Cell ◽  
Dominant Negative ◽  
Neural Tubes ◽  
Dorsal Neural Tube ◽  
Neural Crest Cell Migration ◽  
Fgf Signalling ◽  
Crest Cell

SummaryFibroblast growth factor (FGF) signalling acts as one of modulators that control neural crest cell (NCC) migration, but how this is achieved is still unclear. In this study, we investigated the effects of FGF signalling on NCC migration by blocking this process. Constructs that were capable of inducing Sprouty2 (Spry2) or dominant-negative FGFR1 (Dn-FGFR1) expression were transfected into the cells making up the neural tubes. Our results revealed that blocking FGF signalling at stage HH10 (neurulation stage) could enhance NCC migration at both the cranial and trunk levels in the developing embryos. It was established that FGF-mediated NCC migration was not due to altering the expression of N-cadherin in the neural tube. Instead, we determined that cyclin D1 was overexpressed in the cranial and trunk levels when Sprouty2 was upregulated in the dorsal neural tube. These results imply that the cell cycle was a target of FGF signalling through which it regulates NCC migration at the neurulation stage.

scholarly journals Investigating the role of claudin-1 in neural crest cell migration

2011 ◽  
Vol 356 (1) ◽  
pp. 203
Author(s):  
Theresa E. Neiderer ◽  
Abigail Figat ◽  
Lisa Taneyhill
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Neural Crest Cell Migration ◽  
Crest Cell

Inactivation of the (β)-catenin gene by Wnt1-Cre-mediated deletion results in dramatic brain malformation and failure of craniofacial development

Development ◽  
2001 ◽  
Vol 128 (8) ◽  
pp. 1253-1264 ◽  
Author(s):  
V. Brault ◽  
R. Moore ◽  
S. Kutsch ◽  
M. Ishibashi ◽  
D.H. Rowitch ◽  
...  
Keyword(s):  
Neural Crest ◽  
Wnt Signaling Pathway ◽  
Neural Crest Cell ◽  
Craniofacial Development ◽  
Central Component ◽  
Regulatory Sequences ◽  
Brain Malformation ◽  
Cranial Ganglia ◽  
Crest Cell

('bgr;)-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of (β)-catenin during brain morphogenesis, by specifically inactivating the (β)-catenin gene in the region of Wnt1 expression. To achieve this, mice with a conditional ('floxed') allele of (β)-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of Wnt1 regulatory sequences. (β)-catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional Wnt1 knockout (Wnt1(−)(/)(−)), suggesting that Wnt1 acts through (β)-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack Wnt1, indicates a role for (β)-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (β)-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of (β)-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of (β)-catenin in morphogenetic processes during brain and craniofacial development.

Role of the Extracellular Matrix in Neural Crest Cell Migration

1984 ◽  
pp. 139-144 ◽  
Author(s):  
Jean Paul Thiery ◽  
Roberto Rovasio ◽  
Annie Delouvée ◽  
Michel Vincent ◽  
Jean Loup Duband ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Neural Crest Cell Migration ◽  
Crest Cell

scholarly journals Role of endothelin-A receptor in cardiac neural crest cell fate

2011 ◽  
Vol 356 (1) ◽  
pp. 197-198
Author(s):  
Yanping Zhang ◽  
Mitchell T. McKnight ◽  
L. Bruno Ruest
Keyword(s):  
Neural Crest ◽  
Cell Fate ◽  
Neural Crest Cell ◽  
Cardiac Neural Crest ◽  
Endothelin A Receptor ◽  
Endothelin A ◽  
Crest Cell

scholarly journals TWIST1 and chromatin regulatory proteins interact to guide neural crest cell differentiation

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Xiaochen Fan ◽  
V Pragathi Masamsetti ◽  
Jane QJ Sun ◽  
Kasper Engholm-Keller ◽  
Pierre Osteil ◽  
...  
Keyword(s):  
Neural Crest ◽  
Cell Fate ◽  
Neural Crest Cell ◽  
Regulatory Proteins ◽  
Cellular Functions ◽  
Regulatory Module ◽  
Network Propagation ◽  
High Level ◽  
Craniofacial Tissue ◽  
Crest Cell

Protein interaction is critical molecular regulatory activity underlining cellular functions and precise cell fate choices. Using TWIST1 BioID-proximity-labelling and network propagation analyses, we discovered and characterized a TWIST-chromatin regulatory module (TWIST1-CRM) in the neural crest cells (NCC). Combinatorial perturbation of core members of TWIST1-CRM: TWIST1, CHD7, CHD8, and WHSC1 in cell models and mouse embryos revealed that loss of the function of the regulatory module resulted in abnormal differentiation of NCCs and compromised craniofacial tissue patterning. Following NCC delamination, low level of TWIST1-CRM activity is instrumental to stabilize the early NCC signatures and migratory potential by repressing the neural stem cell programs. High level of TWIST1 module activity at later phases commits the cells to the ectomesenchyme. Our study further revealed the functional interdependency of TWIST1 and potential neurocristopathy factors in NCC development.

Immunohistochemical localisation of chondroitin sulphate proteoglycans and the effects of chondroitinase ABC in 9- to 11-day rat embryos

Development ◽  
1989 ◽  
Vol 106 (4) ◽  
pp. 787-798
Author(s):  
G. Morriss-Kay ◽  
F. Tuckett
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Chondroitin Sulphate ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Neural Tube Closure ◽  
Chondroitinase Abc ◽  
Rat Embryos ◽  
Crest Cell ◽  
Tube Closure

Studies on cell behaviour in vitro have indicated that the chondroitin sulphate proteoglycan (CSPG) family of molecules can participate in the control of cell proliferation, differentiation and adhesion, but its morphogenetic functions had not been investigated in intact embryos. Chondroitin/chondroitin sulphates have been identified in rat embryos at low levels at the start of neurulation (day 9) and at much higher levels on day 10. In this study we have sought evidence for the morphogenetic functions of CSPGs in rat embryos during the period of neurulation and neural crest cell migration by a combination of two approaches: immunocytochemical localization of CSPG by means of an antibody, CS-56, to the chondroitin sulphate component of CSPG, and exposure of embryos to the enzyme chondroitinase ABC. Staining of the CS-56 epitope was poor at the beginning of cranial neurulation; bright staining was at first confined to the primary mesenchyme under the convex neural folds late on day 9. In day 10 embryos, all mesenchyme cells were stained, but at different levels of intensity, so that primary mesenchyme, neural crest and sclerotomal cells could be distinguished from each other. Basement membranes were also stained, particularly bright staining being present where two epithelial were basally apposed, e.g., neural/surface ectoderms, dorsal aorta/neural tube, prior to migration of a population of cells between them. Staining within the neural epithelium was first confined to the dorsolateral edge region, and associated with the onset of neural crest cell emigration; after neural tube closure, neuroepithelial staining was more general. Neural crest cells were stained during migration, but the reaction was absent in areas associated with migration end-points (trigeminal ganglion anlagen, frontonasal mesenchyme). Embryos exposed to chondroitinase ABC in culture showed no abnormalities until early day 10, when cranial neural crest cell emigration from the neural epithelium was inhibited and neural tube closure was retarded. Sclerotomal cells failed to take their normal pathway between the dorsal aorta and neural tube. Correlation of the results of these two methods suggests: (1) that by decreasing adhesiveness within the neural epithelium at specific stages, CSPG facilitates the emigration of neural crest cells and the migratory movement of neuroblasts, and may also provide increased flexibility during the generation of epithelial curvatures; (2) that by decreasing the adhesiveness of fibronectin-containing extracellular matrices, CSPG facilitates the migration of neural crest and sclerotomal cells. This second function is particularly important when migrating cells take pathways between previously apposed tissues.

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