A study of the regulatory roles of Hedgehog in the enteric nervous system development by the conditional knockout of Patched1 enteric gene in the enteric neural crest cells

2009 ◽  
Author(s):  
Hiu-ching Poon
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Enteric Nervous System ◽  
System Development ◽  
Neural Crest Cells ◽  
Nervous System Development ◽  
Conditional Knockout ◽  
Enteric Nervous System Development

scholarly journals Ablation of Ezh2 in neural crest cells leads to aberrant enteric nervous system development in mice

PLoS ONE ◽  
2018 ◽  
Vol 13 (8) ◽  
pp. e0203391
Author(s):  
Hana Kim ◽  
Ingeborg M. Langohr ◽  
Mohammad Faisal ◽  
Margaret McNulty ◽  
Caitlin Thorn ◽  
...  
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Enteric Nervous System ◽  
System Development ◽  
Neural Crest Cells ◽  
Nervous System Development ◽  
Enteric Nervous System Development

scholarly journals Meis3 is required for neural crest invasion of the gut during zebrafish enteric nervous system development

2015 ◽  
Vol 26 (21) ◽  
pp. 3728-3740 ◽  
Author(s):  
Rosa A. Uribe ◽  
Marianne E. Bronner
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Enteric Nervous System ◽  
Molecular Mechanisms ◽  
System Development ◽  
Neural Crest Cells ◽  
Nervous System Development ◽  
Shh Pathway ◽  
Early Migration ◽  
Enteric Nervous System Development

During development, vagal neural crest cells fated to contribute to the enteric nervous system migrate ventrally away from the neural tube toward and along the primitive gut. The molecular mechanisms that regulate their early migration en route to and entry into the gut remain elusive. Here we show that the transcription factor meis3 is expressed along vagal neural crest pathways. Meis3 loss of function results in a reduction in migration efficiency, cell number, and the mitotic activity of neural crest cells in the vicinity of the gut but has no effect on neural crest or gut specification. Later, during enteric nervous system differentiation, Meis3-depleted embryos exhibit colonic aganglionosis, a disorder in which the hindgut is devoid of neurons. Accordingly, the expression of Shh pathway components, previously shown to have a role in the etiology of Hirschsprung’s disease, was misregulated within the gut after loss of Meis3. Taken together, these findings support a model in which Meis3 is required for neural crest proliferation, migration into, and colonization of the gut such that its loss leads to severe defects in enteric nervous system development.

scholarly journals Hoxb3 vagal neural crest-specific enhancer element for controlling enteric nervous system development

2005 ◽  
Vol 233 (2) ◽  
pp. 473-483 ◽  
Author(s):  
Kwok Keung Chan ◽  
Yuk Shan Chen ◽  
Tai On Yau ◽  
Ming Fu ◽  
Vincent Chi Hang Lui ◽  
...  
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Enteric Nervous System ◽  
System Development ◽  
Nervous System Development ◽  
Enhancer Element ◽  
Enteric Nervous System Development

scholarly journals Changes in Nicotinic Neurotransmission during Enteric Nervous System Development

2015 ◽  
Vol 35 (18) ◽  
pp. 7106-7115 ◽  
Author(s):  
J. P. P. Foong ◽  
C. S. Hirst ◽  
M. M. Hao ◽  
S. J. McKeown ◽  
W. Boesmans ◽  
...  
Keyword(s):  
Nervous System ◽  
Enteric Nervous System ◽  
System Development ◽  
Nervous System Development ◽  
Enteric Nervous System Development

scholarly journals Testing the Ret and Sema3d genetic interaction in mouse enteric nervous system development

2017 ◽  
Vol 26 (10) ◽  
pp. 1811-1820 ◽  
Author(s):  
Ashish Kapoor ◽  
Dallas R. Auer ◽  
Dongwon Lee ◽  
Sumantra Chatterjee ◽  
Aravinda Chakravarti
Keyword(s):  
Nervous System ◽  
Enteric Nervous System ◽  
Genetic Interaction ◽  
System Development ◽  
Nervous System Development ◽  
Enteric Nervous System Development

scholarly journals Vitamin E is Necessary to Protect Neural Crest Cells in Developing Zebrafish Embryos

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1209-1209
Author(s):  
Brian Head ◽  
Jane La Du ◽  
Robyn Tanguay ◽  
Chrissa Kioussi ◽  
Maret Traber
Keyword(s):  
Nervous System ◽  
Vitamin E ◽  
Neural Crest ◽  
System Development ◽  
Neural Crest Cells ◽  
Nervous System Development ◽  
Neural Plate ◽  
Zebrafish Embryos ◽  
Normal Brain ◽  
Collagen Formation

Abstract Objectives Vitamin E (VitE) deficiency causes vertebrate embryonic lethality. The alpha-tocopherol transfer protein (Ttpa) likely regulates VitE distribution in the early zebrafish embryo because Ttpa knockdown causes impaired nervous system development and embryonic death by 15–18 hours post-fertilization (hpf). We propose that VitE is necessary for normal brain and peripheral nervous system development. Methods Zebrafish embryos are obtained from adults fed either VitE sufficient (E+) or deficient (E–) diets for at least 80 days. Embryos at 12 and 24 hpf are subjected to RNA whole mount in situ hybridization (WISH). RNA is also collected from embryos at 12, 18 and 24 hpf for RT-qPCR of specific targets. Results At 12 hpf, the midbrain-hindbrain boundary and otic placodes are malformed in E– embryos, as shown by Pax2a expression. Similarly, Sox10 expression shows that E– embryos lack clear neural plate borders. Nonetheless, in 12 hpf E + and E− embryos Ttpa is localized similarly throughout the nervous system. Pax2a expression initiates collagen formation in the developing notochord. Collagen genes, col2a1a and col9a2, expression patterns showed abnormal notochord structures in 24 hpf E– embryos. At 24 hpf in E + embryos, Sox10 expressing-neural crest cells are localized both in the central nervous system and dorsal root ganglia (DRG), while the Sox10 signal is diminished in E– embryos in both the DRG and early enteric nervous system. At 24 hpf, Ttpa expression outlines the brain ventricle borders; critically E– embryos show reduced Ttpa signal and impaired ventricle closing. Gene expression by qPCR will be used to confirm these results. Conclusions This VitE deficient embryo model suggests that the carefully programmed development of the nervous system is distorted due to lack of adequate VitE. Thus, Ttpa and VitE are critical molecules for neural plate and neural tube formation, and neural crest cell migration. Funding Sources The authors received no specific funding for this work.

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