scholarly journals 2SC-02 Coordination of mitosis and morphogenesis : Role of a prolonged G2 phase during chordate neural tube closure(2SC Whole body imaging,The 49th Annual Meeting of the Biophysical Society of Japan)

2011 ◽  
Vol 51 (supplement) ◽  
pp. S15-S16
Author(s):  
Yosuke Ogura ◽  
Asako Sakaue-Sawano ◽  
Masashi Nakagawa ◽  
Nori Satoh ◽  
Atsushi Miyawaki ◽  
...  
Keyword(s):  
Annual Meeting ◽  
Neural Tube ◽  
Neural Tube Closure ◽  
Whole Body ◽  
Whole Body Imaging ◽  
Body Imaging ◽  
Biophysical Society ◽  
G2 Phase ◽  
Tube Closure

scholarly journals 2SC-05 Imaging of structure, development and function of nervous system in a simple vertebrate(2SC Whole body imaging,The 49th Annual Meeting of the Biophysical Society of Japan)

2011 ◽  
Vol 51 (supplement) ◽  
pp. S16
Author(s):  
Kohei Hatta ◽  
Shinichi Okamoto ◽  
Masashi Nakagawa ◽  
Takanori Ikenaga ◽  
Tamami Yamamoto ◽  
...  
Keyword(s):  
Nervous System ◽  
Annual Meeting ◽  
Whole Body ◽  
Whole Body Imaging ◽  
Structure Development ◽  
Body Imaging ◽  
Biophysical Society ◽  
And Function

The Role of Whole-Body Imaging in the Diagnosis, Staging, and Follow-Up of Multiple Myeloma

2010 ◽  
Vol 14 (01) ◽  
pp. 037-046 ◽  
Author(s):  
Conor Shortt ◽  
Fiona Carty ◽  
John Murray
Keyword(s):  
Multiple Myeloma ◽  
Whole Body ◽  
Whole Body Imaging ◽  
Body Imaging

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.

scholarly journals Role of Mammalian Formin Fhod3 in Neural Tube Closure

2018 ◽  
Vol WCP2018 (0) ◽  
pp. PO4-1-52
Author(s):  
Hikmawan W Sulistomo ◽  
Yohko Kage ◽  
Takayuki Nemoto ◽  
Ryu Takeya
Keyword(s):  
Neural Tube ◽  
Neural Tube Closure ◽  
Tube Closure

scholarly journals Insights into the Etiology of Mammalian Neural Tube Closure Defects from Developmental, Genetic and Evolutionary Studies

2018 ◽  
Vol 6 (3) ◽  
pp. 22 ◽  
Author(s):  
Diana Juriloff ◽  
Muriel Harris
Keyword(s):  
Neural Tube ◽  
Gene Mutations ◽  
Neural Tube Closure ◽  
Specific Gene ◽  
New Developments ◽  
Mouse Mutants ◽  
Folate Pathway ◽  
Tube Closure ◽  
Anterior Posterior

The human neural tube defects (NTD), anencephaly, spina bifida and craniorachischisis, originate from a failure of the embryonic neural tube to close. Human NTD are relatively common and both complex and heterogeneous in genetic origin, but the genetic variants and developmental mechanisms are largely unknown. Here we review the numerous studies, mainly in mice, of normal neural tube closure, the mechanisms of failure caused by specific gene mutations, and the evolution of the vertebrate cranial neural tube and its genetic processes, seeking insights into the etiology of human NTD. We find evidence of many regions along the anterior–posterior axis each differing in some aspect of neural tube closure—morphology, cell behavior, specific genes required—and conclude that the etiology of NTD is likely to be partly specific to the anterior–posterior location of the defect and also genetically heterogeneous. We revisit the hypotheses explaining the excess of females among cranial NTD cases in mice and humans and new developments in understanding the role of the folate pathway in NTD. Finally, we demonstrate that evidence from mouse mutants strongly supports the search for digenic or oligogenic etiology in human NTD of all types.

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