scholarly journals Genetic Influences on the Amount of Cell Death in the Neural Tube of BXD Mice Exposed to Acute Ethanol at Midgestation

2019 ◽  
Vol 43 (3) ◽  
pp. 439-452 ◽  
Author(s):  
Emilie T. Théberge ◽  
Jessica A. Baker ◽  
Candis Dubose ◽  
Julia K. Boyle ◽  
Kristina Balce ◽  
...  
Keyword(s):  
Cell Death ◽  
Neural Tube ◽  
Genetic Influences ◽  
Acute Ethanol ◽  
Bxd Mice

scholarly journals Is programmed cell death required for neural tube closure?

1997 ◽  
Vol 7 (4) ◽  
pp. 281-284 ◽  
Author(s):  
Miguel Weil ◽  
Michael D. Jacobson ◽  
Martin C. Raff
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Neural Tube ◽  
Neural Tube Closure ◽  
Tube Closure

Sonic hedgehog is required for survival of both myogenic and chondrogenic somitic lineages

Development ◽  
1998 ◽  
Vol 125 (11) ◽  
pp. 2019-2030 ◽  
Author(s):  
M. Teillet ◽  
Y. Watanabe ◽  
P. Jeffs ◽  
D. Duprez ◽  
F. Lapointe ◽  
...  
Keyword(s):  
Cell Death ◽  
Sonic Hedgehog ◽  
Neural Tube ◽  
Surgical Ablation ◽  
Cell Lineages ◽  
Ventral Neural Tube ◽  
Close Relationship ◽  
Body Wall Muscles ◽  
Epaxial Muscles ◽  
Axial Organs

In vertebrates, the medial moieties of the somites give rise to the vertebrae and epaxial muscles, which develop in close relationship with the axial organs, neural tube and notochord. The lateral moieties contribute to the ribs and to limb and body wall muscles (hypaxial muscles) after a phase of lateral and ventral migration. Surgical ablation of the neural tube and notochord in the chick embryo during segmentation and early differentiation of the somites (day 2 of incubation) does not affect primary development of the hypaxial muscles, but leads to a complete absence of epaxial muscles, vertebrae and ribs, due to cell death in the somites. Here we demonstrate that cell death, which occurs within 24 hours of excision of the axial organs, affects both myogenic and chondrogenic cell lineages defined, respectively, by the expression of MyoD and Pax-1 genes. In contrast, Pax-3 transcripts, normally present in cells giving rise to hypaxial muscles, are preserved in the excised embryos. Backgrafting either the ventral neural tube or the notochord allows survival of MyoD- and Pax-1-expressing cells. Similarly, Sonic hedgehog-producing cells grafted in place of axial organs also rescue MyoD- and Pax-1-expressing cells from death and allow epaxial muscles, ribs and vertebrae to undergo organogenesis. These results demonstrate that the ventral neural tube and the notochord promote the survival of both myogenic and chondrogenic cell lineages in the somites and that this action is mediated by Sonic hedgehog.

scholarly journals Formation of neurodegenerative aggresome and death-inducing signaling complex in maternal diabetes-induced neural tube defects

2017 ◽  
Vol 114 (17) ◽  
pp. 4489-4494 ◽  
Author(s):  
Zhiyong Zhao ◽  
Lixue Cao ◽  
E. Albert Reece
Keyword(s):  
Cell Death ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Protein Misfolding ◽  
Maternal Diabetes ◽  
Misfolded Proteins ◽  
Caspase 8 ◽  
Signaling Complex

Diabetes mellitus in early pregnancy increases the risk in infants of birth defects, such as neural tube defects (NTDs), known as diabetic embryopathy. NTDs are associated with hyperglycemia-induced protein misfolding and Caspase-8–induced programmed cell death. The present study shows that misfolded proteins are ubiquitinylated, suggesting that ubiquitin-proteasomal degradation is impaired. Misfolded proteins form aggregates containing ubiquitin-binding protein p62, suggesting that autophagic-lysosomal clearance is insufficient. Additionally, these aggregates contain the neurodegenerative disease-associated proteins α-Synuclein, Parkin, and Huntingtin (Htt). Aggregation of Htt may lead to formation of a death-inducing signaling complex of Hip1, Hippi, and Caspase-8. Treatment with chemical chaperones, such as sodium 4-phenylbutyrate (PBA), reduces protein aggregation in neural stem cells in vitro and in embryos in vivo. Furthermore, treatment with PBA in vivo decreases NTD rate in the embryos of diabetic mice, as well as Caspase-8 activation and cell death. Enhancing protein folding could be a potential interventional approach to preventing embryonic malformations in diabetic pregnancies.

scholarly journals Mouse Fkbp8 activity is required to inhibit cell death and establish dorso-ventral patterning in the posterior neural tube

2007 ◽  
Vol 17 (4) ◽  
pp. 587-601 ◽  
Author(s):  
Rebecca Lee Yean Wong ◽  
Bogdan J. Wlodarczyk ◽  
Kyung Soo Min ◽  
Melissa L. Scott ◽  
Susan Kartiko ◽  
...  
Keyword(s):  
Cell Death ◽  
Neural Tube

Anti-apoptotic role of Sonic hedgehog protein at the early stages of nervous system organogenesis

Development ◽  
2001 ◽  
Vol 128 (20) ◽  
pp. 4011-4020 ◽  
Author(s):  
Jean-Baptiste Charrier ◽  
Françoise Lapointe ◽  
Nicole M. Le Douarin ◽  
Marie-Aimée Teillet
Keyword(s):  
Cell Death ◽  
Nervous System ◽  
Chick Embryo ◽  
Sonic Hedgehog ◽  
Neural Tube ◽  
Primitive Streak ◽  
Embryo Cell ◽  
Floor Plate ◽  
Cell Death Program ◽  
Midline Cells

In vertebrates the neural tube, like most of the embryonic organs, shows discreet areas of programmed cell death at several stages during development. In the chick embryo, cell death is dramatically increased in the developing nervous system and other tissues when the midline cells, notochord and floor plate, are prevented from forming by excision of the axial-paraxial hinge (APH), i.e. caudal Hensen’s node and rostral primitive streak, at the 6-somite stage (Charrier, J. B., Teillet, M.-A., Lapointe, F. and Le Douarin, N. M. (1999). Development126, 4771-4783). In this paper we demonstrate that one day after APH excision, when dramatic apoptosis is already present in the neural tube, the latter can be rescued from death by grafting a notochord or a floor plate fragment in its vicinity. The neural tube can also be recovered by transplanting it into a stage-matched chick embryo having one of these structures. In addition, cells engineered to produce Sonic hedgehog protein (SHH) can mimic the effect of the notochord and floor plate cells in in situ grafts and transplantation experiments. SHH can thus counteract a built-in cell death program and thereby contribute to organ morphogenesis, in particular in the central nervous system.

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