O26. Role of cell division during neural tube formation in the zebrafish

2010 ◽  
Vol 80 ◽  
pp. S13-S14
Author(s):  
Una Ren ◽  
Gemma Girdler ◽  
Clare Buckley ◽  
Jon Clarke
Keyword(s):  
Cell Division ◽  
Neural Tube ◽  
Tube Formation ◽  
Neural Tube Formation

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.

The role of F-cadherin in localizing cells during neural tube formation in Xenopus embryos

Development ◽  
1998 ◽  
Vol 125 (2) ◽  
pp. 301-312 ◽  
Author(s):  
A. Espeseth ◽  
G. Marnellos ◽  
C. Kintner
Keyword(s):  
Cell Adhesion ◽  
Neural Tube ◽  
Cell Adhesion Molecule ◽  
Ectopic Expression ◽  
Tube Formation ◽  
Cell Movements ◽  
Xenopus Embryos ◽  
Extensive Cell ◽  
Neural Tube Formation

The cell adhesion molecule F-cadherin is expressed in Xenopus embryos at boundaries that subdivide the neural tube into different regions, including one, the sulcus limitans, which partitions the caudal neural tube into a dorsal and ventral half (alar and basal plate, respectively). Here we examine the role of F-cadherin in positioning cells along the caudal neuraxis during neurulation. First, we show that ectopic expression of F-cadherin restricts passive cell mixing within the ectodermal epithelium. Second, we show that F-cadherin is first expressed at the sulcus limitans prior to the extensive cell movements that accompany neural tube formation, suggesting that it might serve to position cells at the sulcus limitans by counteracting their tendency to disperse during neurulation. We test this idea using an assay that measures changes in cell movements during neurulation in response to differential cell adhesion. Using this assay, we show that cells expressing F-cadherin localize preferentially to the sulcus limitans, but still disperse when located away from the sulcus limitans. In addition, inhibiting cadherin function prevents cells from localizing precisely at the sulcus limitans. These results indicate that positioning of cells at the sulcus limitans is mediated in part by the differential expression of F-cadherin.

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 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 partially rescue neurogenesis. To further investigate the developmental role of p120ctn in neural tube formation, we generated conditional p120ctn fl/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 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.

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.

Sign in / Sign up

Export Citation Format

Share Document