Central role of the ?4?1 integrin in the coordination of avian truncal neural crest cell adhesion, migration, and survival

2001 ◽  
Vol 222 (2) ◽  
pp. 127-140 ◽  
Author(s):  
Sandrine Testaz ◽  
Jean-Loup Duband
Keyword(s):  
Cell Adhesion ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Crest Cell

Role of collagen and fibronectin in neural crest cell adhesion and migration

1981 ◽  
Vol 87 (2) ◽  
pp. 259-266 ◽  
Author(s):  
Judith H. Greenberg ◽  
Silja Seppä ◽  
Heikki Seppä ◽  
A.Tyl Hewitt
Keyword(s):  
Cell Adhesion ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Cell Adhesion And Migration ◽  
And Migration ◽  
Crest Cell

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 Neural crest cell migration: requirements for exogenous fibronectin and high cell density.

1983 ◽  
Vol 96 (2) ◽  
pp. 462-473 ◽  
Author(s):  
R A Rovasio ◽  
A Delouvee ◽  
K M Yamada ◽  
R Timpl ◽  
J P Thiery
Keyword(s):  
Cell Adhesion ◽  
Neural Crest ◽  
Type I Collagen ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Type I ◽  
Cell Adhesion And Migration ◽  
And Migration ◽  
Crest Cell

Cells of the neural crest participate in a major class of cell migratory events during embryonic development. From indirect evidence, it has been suggested that fibronectin (FN) might be involved in these events. We have directly tested the role of FN in neural crest cell adhesion and migration using several in vitro model systems. Avian trunk neural crest cells adhered readily to purified plasma FN substrates and to extracellular matrices containing cellular FN. Their adhesion was inhibited by antibodies to a cell-binding fragment of FN. In contrast, these cells did not adhere to glass, type I collagen, or to bovine serum albumin in the absence of FN. Neural crest cell adhesion to laminin (LN) was significantly less than to FN; however, culturing of crest cells under conditions producing an epithelioid phenotype resulted in cells that could bind equally as well to LN as to FN. The migration of neural crest cells appeared to depend on both the substrate and the extent of cell interactions. Cells migrated substantially more rapidly on FN than on LN or type I collagen substrates; if provided a choice between stripes of FN and glass or LN, cells migrated preferentially on the FN. Migration was inhibited by antibodies against the cell-binding region of FN, and the inhibition could be reversed by a subsequent addition of exogenous FN. However, the migration on FN was random and displayed little persistence of direction unless cells were at high densities that permitted frequent contacts. The in vitro rate of migration of cells on FN-containing matrices was 50 microns/h, similar to their migration rates along the narrow regions of FN-containing extracellular matrix in migratory pathways in vivo. These results indicate that FN is important for neural crest cell adhesion and migration and that the high cell densities of neural crest cells in the transient, narrow migratory pathways found in the embryo are necessary for effective directional migration.

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
Sign in / Sign up

Export Citation Format

Share Document