Lipid droplets of neuroepithelial cells are a major calcium storage site during neural tube formation in chick and mouse embryos

1992 ◽  
Vol 48 (5) ◽  
pp. 516-519 ◽  
Author(s):  
K. T. Bush ◽  
H. Lee ◽  
R. G. Nagele
Keyword(s):  
Neural Tube ◽  
Lipid Droplets ◽  
Tube Formation ◽  
Mouse Embryos ◽  
Storage Site ◽  
Calcium Storage ◽  
Neuroepithelial Cells ◽  
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

Abnormal neural fold development in trisomy 12 and trisomy 14 mouse embryos

Development ◽  
1981 ◽  
Vol 66 (1) ◽  
pp. 141-158
Author(s):  
Barbara Putz ◽  
Gillian Morriss-Kay
Keyword(s):  
Neural Tube ◽  
Anterior Part ◽  
Tube Formation ◽  
Mouse Embryos ◽  
Somite Stage ◽  
Mammalian Embryos ◽  
Trisomy 12 ◽  
Optic Vesicles ◽  
Normal Laboratory ◽  
Neural Tube Formation

The early development of the exencephalic malformation in trisomy 12 (Tsl2) and trisomy 14 (Tsl4) mouse embryos was examined by means of scanning electron microscopy and compared with cranial neural tube formation in euploid litter-mates. Embryos from normal laboratory mice were used as additional controls. The euploid control embryos of the trisomy-inducing breeding system showed a slight delay and some variation in the timing of cranial neurulation. The pre-exencephalic trisomic embryos showed hypoplasia, and lower somite number when compared with euploid littermates; there was also a retardation of development of the whole neural tube, when related to the somite stage. External differences from the control embryos were observed at the late pre-somite stage, when the anterior part of the neural plate showed a crumpled appearance. At 6 somites the lateral edges of the forebrain were everted instead of elevated in Tsl2 and Tsl4 embryos. At later stages, however, the forebrain showed a tendency towards the normal morphogenetic pattern, so that the optic vesicles were eventually formed and the most anterior part fused. The caudal forebrain and the midbrain were more permanently affected by the disturbance of trisomic conditions and grew laterally, failing to appose or fuse in the midline in both Tsl2 and Tsl4 embryos. Hindbrain morphogenesis was different in Tsl2 and Tsl4 excencephaly: in Tsl2 embryos it did not close rostral to the otic pits, whereas in Tsl4 embryos it showed a normal closure up to the hindbrain/midbrain junction. These observations support the hypothesis that in mammalian embryos the mechanism of neural tube formation of the future brain region is more complex than that of the spinal neural tube and therefore may be more likely to react to a general delay of neurulation with a gross malformation. Tsl2 and Tsl4 exencephaly are due to a primary non-closure of the neural tube.

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

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.

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