Morphogenetic movements during axolotl neural tube formation tracked by digital imaging

1996 ◽  
Vol 205 (5-6) ◽  
pp. 311-318 ◽  
Author(s):  
G. Wayne Brodland ◽  
Michael J. Scott ◽  
Andrew F. MacLean ◽  
M. Globus ◽  
S. Vethamany-Globus ◽  
...  
Keyword(s):  
Neural Tube ◽  
Digital Imaging ◽  
Tube Formation ◽  
Morphogenetic Movements ◽  
Neural Tube Formation

The Effects of β-Mercaptoethanol on the Morphogenetic Movements of Amphibian Embryos

Development ◽  
1963 ◽  
Vol 11 (1) ◽  
pp. 155-166
Author(s):  
P. Malpoix ◽  
J. Quertier ◽  
J. Brachet
Keyword(s):  
Neural Tube ◽  
Tube Formation ◽  
Animal Pole ◽  
Morphogenetic Movements ◽  
Complete Development ◽  
Early Stages ◽  
Amphibian Embryos ◽  
Biological Specificity ◽  
Neural Tube Formation

The inhibition by β-mercaptoethanol of morphogenesis in amphibians, freshwater hydra, planarians and regenerating tadpoles, has already been reported by one of us (Brachet, 1958, 1959a, b, c). The present work provides a closer analysis of the biological specificity of j8-mercaptoethanol with regard to the different movements which produce gastrulation in amphibians: invagination, epiboly, convergent stretching and ingression. The main result, obtained with Pleurodeles, was that gastrulation is completely inhibited by M/100 β-mercaptoethanol. Lower concentrations (M/300) permit more complete development, but the resulting embryos are abnormal. β-Mercaptoethanol interferes with neural tube formation, but has less effect on the development of the notochord and the mesodermal somites. It was further noted that, when embryos are treated at very early stages (1–2 cells, young blastulae), the blastocoele seems to collapse and the ectoblast of the animal pole is deeply puckered.

scholarly journals Strategies of vertebrate neurulation and a re-evaluation of teleost neural tube formation

2004 ◽  
Vol 121 (10) ◽  
pp. 1189-1197 ◽  
Author(s):  
Laura Anne Lowery ◽  
Hazel Sive
Keyword(s):  
Neural Tube ◽  
Tube Formation ◽  
Neural Tube Formation

scholarly journals Apical Accumulation of Rho in the Neural Plate Is Important for Neural Plate Cell Shape Change and Neural Tube Formation

2008 ◽  
Vol 19 (5) ◽  
pp. 2289-2299 ◽  
Author(s):  
Nagatoki Kinoshita ◽  
Noriaki Sasai ◽  
Kazuyo Misaki ◽  
Shigenobu Yonemura
Keyword(s):  
Neural Tube ◽  
Rho Gtpases ◽  
Cell Shape ◽  
Shape Change ◽  
Myosin Ii ◽  
Tube Formation ◽  
Neural Plate ◽  
Cell Shape Change ◽  
Neural Tube Formation

Although Rho-GTPases are well-known regulators of cytoskeletal reorganization, their in vivo distribution and physiological functions have remained elusive. In this study, we found marked apical accumulation of Rho in developing chick embryos undergoing folding of the neural plate during neural tube formation, with similar accumulation of activated myosin II. The timing of accumulation and biochemical activation of both Rho and myosin II was coincident with the dynamics of neural tube formation. Inhibition of Rho disrupted its apical accumulation and led to defects in neural tube formation, with abnormal morphology of the neural plate. Continuous activation of Rho also altered neural tube formation. These results indicate that correct spatiotemporal regulation of Rho is essential for neural tube morphogenesis. Furthermore, we found that a key morphogenetic signaling pathway, the Wnt/PCP pathway, was implicated in the apical accumulation of Rho and regulation of cell shape in the neural plate, suggesting that this signal may be the spatiotemporal regulator of Rho in neural tube formation.

scholarly journals Folate Infuence Wnt, Beta-catenin, and Cadherin Pathways during Neural Tube Formation(Extended abstract)

2008 ◽  
Vol 22 (2) ◽  
pp. 119-121
Author(s):  
Yasuomi Nonaka ◽  
Yuzaburo Shimizu ◽  
Osamu Akiyama ◽  
Satoshi Tsutsumi ◽  
Yusuke Abe ◽  
...  
Keyword(s):  
Neural Tube ◽  
Tube Formation ◽  
Beta Catenin ◽  
Neural Tube Formation

Abnormalities of neural tube formation in pre-spina bifida splotch-delayed mouse embryos

Teratology ◽  
1991 ◽  
Vol 43 (6) ◽  
pp. 643-657 ◽  
Author(s):  
Xiu-Ming Yang ◽  
Daphne G. Trasler
Keyword(s):  
Spina Bifida ◽  
Neural Tube ◽  
Tube Formation ◽  
Mouse Embryos ◽  
Neural Tube Formation

scholarly journals Cell intercalation driven by SMAD3 underlies secondary neural tube formation

2020 ◽  
Author(s):  
Elena Gonzalez-Gobartt ◽  
José Blanco-Ameijeiras ◽  
Susana Usieto ◽  
Guillaume Allio ◽  
Bertrand Benazeraf ◽  
...  
Keyword(s):  
Neural Tube ◽  
Epithelial To Mesenchymal Transition ◽  
De Novo ◽  
Tube Formation ◽  
List Type ◽  
Lumen Formation ◽  
Mesenchymal Transition ◽  
Cell Intercalation ◽  
Neural Tube Formation

SUMMARYBody axis elongation is a hallmark of the vertebrate embryo, involving the architectural remodelling of the tailbud. Although it is clear how bi-potential neuro-mesodermal progenitors (NMPs) contribute to embryo elongation, the dynamic events that lead to de novo lumen formation and that culminate in the formation of a 3-Dimensional, secondary neural tube from NMPs, are poorly understood. Here, we used in vivo imaging of the chicken embryo to show that cell intercalation downstream of TGF-beta/SMAD3 signalling is required for secondary neural tube formation. Our analysis describes the initial events in embryo elongation including lineage restriction, the epithelial-to-mesenchymal transition of NMPs, and the initiation of lumen formation. Importantly, we show that the resolution of a single, centrally positioned continuous lumen, which occurs through the intercalation of central cells, requires SMAD3 activity. We anticipate that these findings will be relevant to understand caudal, skin-covered neural tube defects, amongst the most frequent birth defects detected in humans.HIGHLIGHTS.- Initiation of the lumen formation follows the acquisition of neural identity and epithelial polarization..- Programmed cell death is not required for lumen resolution..- Resolution of a single central lumen requires cell intercalation, driven by Smad3 activity.- The outcome of central cell division preceding cell intercalation, varies along the cranio-caudal axis.

scholarly journals Neural Defects Caused by Total and Wnt1-Cre Mediated Ablation of p120ctn in Mice

2020 ◽  
Author(s):  
Tim Pieters ◽  
Ellen Sanders ◽  
Huiyu Tian ◽  
Jolanda van Hengel ◽  
Frans Van Roy
Keyword(s):  
Cell Adhesion ◽  
Neural Tube ◽  
Tube Formation ◽  
Neural Tube Closure ◽  
Actin Binding ◽  
Apical Side ◽  
Developmental Role ◽  
Tube Closure ◽  
Neural Tube Formation

Abstract Background p120 catenin (p120ctn) is an important component in the cadherin-catenin cell adhesion complex because it stabilizes cadherin-mediated intercellular junctions. Outside these junctions, p120ctn is actively involved in the regulation of small GTPases of the Rho family, in actomyosin dynamics and in transcription regulation. We and others reported that loss of p120ctn in mouse embryos results in an embryonic lethal phenotype, but the exact developmental role of p120ctn during brain formation has not been reported.Results We used Cre/loxP technology to achieve full or tissue-specific deletion of p120ctn in the developing embryo. We combined floxed p120ctn mice with Del-Cre or Wnt1-Cre mice to deplete p120ctn from either all cells or specific brain and neural crest cells. Complete loss of p120ctn in mid-gestation embryos resulted in an aberrant morphology, including growth retardation, failure to switch from lordotic to fetal posture, and defective neural tube formation and neurogenesis. By expressing a wild-type p120ctn from the ROSA26 locus in p120ctn-null mouse embryonic stem cells, we could recapitulate neurogenesis and partially rescue neurogenesis. To further investigate the developmental role of p120ctn in neural tube formation, we generated conditional p120ctnfl/fl;Wnt1Cre knockout mice. p120ctn deletion in Wnt1-expressing cells resulted in neural tube closure defects (NTDs) and craniofacial abnormalities. These defects could not be correlated with misregulation of brain marker genes or cell proliferation. In contrast, we found that p120ctn is required for proper expression of the cell adhesion components N-cadherin, E-cadherin and β-catenin, and of actin-binding proteins cortactin and Shroom3 at the apical side of neural folds. This region is of critical importance for closure of neural folds. Surprisingly, the lateral side of mutant neural folds showed loss of p120ctn, but not of N-cadherin, β-catenin or cortactin.Conclusions These results indicate that p120ctn is strictly required for neurogenesis and neurulation. Elimination of p120ctn in cells expressing Wnt1 affects neural tube closure by hampering correct formation of specific adhesion and actomyosin complexes at the apical side of neural folds. Collectively, our results demonstrate the crucial role of p120ctn during brain morphogenesis.

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