Migratory Neural Crest Cells Phagocytose Cellular Debris in the Developing Nervous System

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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Enteric nervous system formation: disproportionate stochastic clonal expansion of a few initiating vagal neural crest cells

Mechanisms of Development ◽

10.1016/j.mod.2017.04.061 ◽

2017 ◽

Vol 145 ◽

pp. S40-S41

Author(s):

Donald Newgreen ◽

Dongcheng Zhang ◽

James Osborne ◽

Bevan Cheeseman ◽

Benjamin Binder ◽

...

Keyword(s):

Nervous System ◽

Neural Crest ◽

Enteric Nervous System ◽

Neural Crest Cells ◽

Clonal Expansion ◽

System Formation

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Chick Sox10, a transcription factor expressed in both early neural crest cells and central nervous system

Developmental Brain Research ◽

10.1016/s0165-3806(00)00049-3 ◽

2000 ◽

Vol 121 (2) ◽

pp. 233-241 ◽

Cited By ~ 111

Author(s):

Yi-Chuan Cheng ◽

Martin Cheung ◽

Muhammad M. Abu-Elmagd ◽

Alex Orme ◽

Paul J. Scotting

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Transcription Factor ◽

Neural Crest ◽

Neural Crest Cells

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Vital dye labelling demonstrates a sacral neural crest contribution to the enteric nervous system of chick and mouse embryos

Development ◽

10.1242/dev.111.4.857 ◽

1991 ◽

Vol 111 (4) ◽

pp. 857-866 ◽

Cited By ~ 13

Author(s):

G.N. Serbedzija ◽

S. Burgan ◽

S.E. Fraser ◽

M. Bronner-Fraser

Keyword(s):

Nervous System ◽

Neural Crest ◽

Enteric Nervous System ◽

Neural Tube ◽

Neural Crest Cells ◽

Mouse Embryos ◽

Chick Embryos ◽

Vital Dye ◽

Dorsal Portion ◽

Sacral Neural Crest

We have used the vital dye, DiI, to analyze the contribution of sacral neural crest cells to the enteric nervous system in chick and mouse embryos. In order to label premigratory sacral neural crest cells selectively, DiI was injected into the lumen of the neural tube at the level of the hindlimb. In chick embryos, DiI injections made prior to stage 19 resulted in labelled cells in the gut, which had emerged from the neural tube adjacent to somites 29–37. In mouse embryos, neural crest cells emigrated from the sacral neural tube between E9 and E9.5. In both chick and mouse embryos, DiI-labelled cells were observed in the rostral half of the somitic sclerotome, around the dorsal aorta, in the mesentery surrounding the gut, as well as within the epithelium of the gut. Mouse embryos, however, contained consistently fewer labelled cells than chick embryos. DiI-labelled cells first were observed in the rostral and dorsal portion of the gut. Paralleling the maturation of the embryo, there was a rostral-to-caudal sequence in which neural crest cells populated the gut at the sacral level. In addition, neural crest cells appeared within the gut in a dorsal-to-ventral sequence, suggesting that the cells entered the gut dorsally and moved progressively ventrally. The present results resolve a long-standing discrepancy in the literature by demonstrating that sacral neural crest cells in both the chick and mouse contribute to the enteric nervous system in the postumbilical gut.

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Faculty Opinions recommendation of Trans-mesenteric neural crest cells are the principal source of the colonic enteric nervous system.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.717961689.793464446 ◽

2012 ◽

Author(s):

Jean-François Brunet

Keyword(s):

Nervous System ◽

Neural Crest ◽

Enteric Nervous System ◽

Neural Crest Cells ◽

Principal Source

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Mesenteric Paraganglioma

Archives of Pathology & Laboratory Medicine ◽

10.5858/2002-126-0362-mp ◽

2002 ◽

Vol 126 (3) ◽

pp. 362-364 ◽

Cited By ~ 2

Author(s):

Shabnam Jaffer ◽

Noam Harpaz

Keyword(s):

Nervous System ◽

Autonomic Nervous System ◽

Neural Crest ◽

Case Reports ◽

Neural Crest Cells ◽

Mesenteric Arteries ◽

Cervical Region ◽

Upper Cervical ◽

Embryologic Development ◽

Extra Adrenal Paraganglioma

Abstract Approximately 5% to 10% of paragangliomas occur in extra-adrenal sites, which can extend from the upper cervical region to the pelvis, parallel to the autonomic nervous system. This distribution corresponds to the embryologic development of the paraganglia from neural crest cells. Rarely, extra-adrenal paragangliomas can also occur aberrantly outside this distribution. We report such a case of extra-adrenal paraganglioma occurring in the anterior mesentery in a 76-year-old man. Two case reports exist in the literature describing extra-adrenal paragangliomas in the posterior mesentery. Normal paraganglionic tissue has been described at the roots of the superior and inferior mesenteric arteries, theoretically explaining the origin of the posterior mesenteric paragangliomas. Our case can best be attributed to the ventral migration of paraganglionic tissue through these vessels to reach the anterior mesentery, where they could potentially give rise to paragangliomas in this site.

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