Localisation et durée des potentialités médullo-surrénaliennes des crêtes neurales chez l'embryon de Poulet

Development ◽  
1972 ◽  
Vol 27 (3) ◽  
pp. 603-614
Author(s):  
Alain Chevallier

The localization and duration of the capacity of neural crest cells to differentiate into medullary cells of the adrenal gland The capacity of the neural crest cells to differentiate into medullary cells of the adrenal gland has been tested for different levels of the cephalo-caudal axis of the chick embryo and at different stages. The procedure consisted in associating a fragment of neural crest cells containing spinal cord with a section of an embryo containing the prospective cortical territory. The latter was previously deprived in ovo of presumptive medullar adrenal cells by localized X-irradiation of its spinal cord. The portion of the spinal cord which has the capacity to give off medulloblasts is located not only within the prospective adrenal area (somite levels 18–22), but also within a region extending over a length of six somites in front and seven somites behind the presumptive zone. This capacity, which is restricted in space, is also limited in time. It is possessed by the portion of spinal cord defined above from 6 h before the migration of the first neural crest cells and lasts roughly for 24 h after the beginning of migration. Furthermore, the experiments indicate that the differentiation of neural crest cells into medullocytes requires the inductive influence of the cortical cells.

Development ◽  
2000 ◽  
Vol 127 (6) ◽  
pp. 1161-1172 ◽  
Author(s):  
P.M. Kulesa ◽  
S.E. Fraser

Hindbrain neural crest cells were labeled with DiI and followed in ovo using a new approach for long-term time-lapse confocal microscopy. In ovo imaging allowed us to visualize neural crest cell migration 2–3 times longer than in whole embryo explant cultures, providing a more complete picture of the dynamics of cell migration from emergence at the dorsal midline to entry into the branchial arches. There were aspects of the in ovo neural crest cell migration patterning which were new and different. Surprisingly, there was contact between neural crest cell migration streams bound for different branchial arches. This cell-cell contact occurred in the region lateral to the otic vesicle, where neural crest cells within the distinct streams diverted from their migration pathways into the branchial arches and instead migrated around the otic vesicle to establish a contact between streams. Some individual neural crest cells did appear to cross between the streams, but there was no widespread mixing. Analysis of individual cell trajectories showed that neural crest cells emerge from all rhombomeres (r) and sort into distinct exiting streams adjacent to the even-numbered rhombomeres. Neural crest cell migration behaviors resembled the wide diversity seen in whole embryo chick explants, including chain-like cell arrangements; however, average in ovo cell speeds are as much as 70% faster. To test to what extent neural crest cells from adjoining rhombomeres mix along migration routes and within the branchial arches, separate groups of premigratory neural crest cells were labeled with DiI or DiD. Results showed that r6 and r7 neural crest cells migrated to the same spatial location within the fourth branchial arch. The diversity of migration behaviors suggests that no single mechanism guides in ovo hindbrain neural crest cell migration into the branchial arches. The cell-cell contact between migration streams and the co-localization of neural crest cells from adjoining rhombomeres within a single branchial arch support the notion that the pattern of hindbrain neural crest cell migration emerges dynamically with cell-cell communication playing an important guidance role.


2021 ◽  
Vol 30 ◽  
pp. 096368972098824
Author(s):  
Iwan Jones ◽  
Liudmila N. Novikova ◽  
Mikael Wiberg ◽  
Leif Carlsson ◽  
Lev N. Novikov

Spinal cord injury results in irreversible tissue damage and permanent sensorimotor impairment. The development of novel therapeutic strategies that improve the life quality of affected individuals is therefore of paramount importance. Cell transplantation is a promising approach for spinal cord injury treatment and the present study assesses the efficacy of human embryonic stem cell–derived neural crest cells as preclinical cell-based therapy candidates. The differentiated neural crest cells exhibited characteristic molecular signatures and produced a range of biologically active trophic factors that stimulated in vitro neurite outgrowth of rat primary dorsal root ganglia neurons. Transplantation of the neural crest cells into both acute and chronic rat cervical spinal cord injury models promoted remodeling of descending raphespinal projections and contributed to the partial recovery of forelimb motor function. The results achieved in this proof-of-concept study demonstrates that human embryonic stem cell–derived neural crest cells warrant further investigation as cell-based therapy candidates for the treatment of spinal cord injury.


2008 ◽  
Vol 19 (4) ◽  
pp. 1575-1586 ◽  
Author(s):  
Simone Reiprich ◽  
C. Claus Stolt ◽  
Silke Schreiner ◽  
Rosanna Parlato ◽  
Michael Wegner

Sry-box (Sox)8, Sox9, and Sox10 are all strongly expressed in the neural crest. Here, we studied the influence of these closely related transcription factors on the developing adrenal medulla as one prominent neural crest derivative. Whereas Sox9 was not expressed, both Sox8 and Sox10 occurred widely in neural crest cells migrating to the adrenal gland and in the gland itself, and they were down-regulated in cells expressing catecholaminergic traits. Sox10-deficient mice lacked an adrenal medulla. The adrenal anlage was never colonized by neural crest cells, which failed to specify properly at the dorsal aorta and died apoptotically during migration. Furthermore, mutant neural crest cells did not express Sox8. Strong adrenal phenotypes were also observed when the Sox10 dimerization domain was inactivated or when a transactivation domain in the central portion was deleted. Sox8 in contrast had only minimal influence on adrenal gland development. Phenotypic consequences became only visible in Sox8-deficient mice upon additional deletion of one Sox10 allele. Replacement of Sox10 by Sox8, however, led to significant rescue of the adrenal medulla, indicating that functional differences between the two related Sox proteins contribute less to the different adrenal phenotypes of the null mutants than dependence of Sox8 expression on Sox10.


No tissue representing the cortex of the adrenal gland has yet been described in the Dipnoi, though it is known in elasmobranchs and in all tetrapod vertebrates. In the mammalian adrenal, lipine-containing inclusions give the cortical cells a char­acteristic appearance at certain stages of their life history. All those viscera of Protopterus which might be suspected of containing cortical tissue were studied in sections by a histo-chemical technique specific for phospholipines. Large intracellular droplets containing phospholipine were demonstrated in a tissue widely distributed around the kidneys, gonads and dorsal aorta throughout the body cavity. The medullary homologue was identified by the chromaffin reaction, and proved to lie, as stated by Giacomini, in the walls of the intercostal branches of the dorsal aorta. The innerva­tion of these medullary cells, from the sympathetic chains, was demonstrated by a silver method. It is suggested that the lipine-containing tissue is that which became the cortex of tetrapods. Its distribution in Protopterus, and its relations with the medullary cells, are such that the elasmobranch and tetrapod adrenals could be derived from it by varying degrees of suppression and migration of the tissues. Amongst Amphibia the adrenal of the Gymnophiona is most similar in arrangement to that of Protopterus . The lipine tissue is so situated as to be readily available for biochemical and endocrinological studies.


2020 ◽  
pp. 69-71
Author(s):  
Farhana Zakaria ◽  
Altaf Khan ◽  
Rahul Bhargava

Adrenal Ganglioneuromas are uncommon tumours arising from neural crest cells in posterior mediastinum and retroperitoneum. Rarely do they arise from adrenal gland and most of them are incidentally detected and hormonally inactive. Radiologically, they appear as any other adrenal mass, hence histopathological examination and immunohistochemistry plays a major role. With the advent of laparoscopy and robot, outcome of surgical treatment has improved a lot.


eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Hironobu Okuno ◽  
Francois Renault Mihara ◽  
Shigeki Ohta ◽  
Kimiko Fukuda ◽  
Kenji Kurosawa ◽  
...  

CHARGE syndrome is caused by heterozygous mutations in the chromatin remodeler, CHD7, and is characterized by a set of malformations that, on clinical grounds, were historically postulated to arise from defects in neural crest formation during embryogenesis. To better delineate neural crest defects in CHARGE syndrome, we generated induced pluripotent stem cells (iPSCs) from two patients with typical syndrome manifestations, and characterized neural crest cells differentiated in vitro from these iPSCs (iPSC-NCCs). We found that expression of genes associated with cell migration was altered in CHARGE iPSC-NCCs compared to control iPSC-NCCs. Consistently, CHARGE iPSC-NCCs showed defective delamination, migration and motility in vitro, and their transplantation in ovo revealed overall defective migratory activity in the chick embryo. These results support the historical inference that CHARGE syndrome patients exhibit defects in neural crest migration, and provide the first successful application of patient-derived iPSCs in modeling craniofacial disorders.


2021 ◽  
Vol 9 (3) ◽  
pp. 30
Author(s):  
Takuma Shinozuka ◽  
Shinji Takada

The most dorsal region, or roof plate, is the dorsal organizing center of developing spinal cord. This region is also involved in development of neural crest cells, which are the source of migratory neural crest cells. During early development of the spinal cord, roof plate cells secrete signaling molecules, such as Wnt and BMP family proteins, which regulate development of neural crest cells and dorsal spinal cord. After the dorso-ventral pattern is established, spinal cord dynamically changes its morphology. With this morphological transformation, the lumen of the spinal cord gradually shrinks to form the central canal, a cavity filled with cerebrospinal fluid that is connected to the ventricular system of the brain. The dorsal half of the spinal cord is separated by a glial structure called the dorsal (or posterior) median septum. However, underlying mechanisms of such morphological transformation are just beginning to be understood. Recent studies reveal that roof plate cells dramatically stretch along the dorso-ventral axis, accompanied by reduction of the spinal cord lumen. During this stretching process, the tips of roof plate cells maintain contact with cells surrounding the shrinking lumen, eventually exposed to the inner surface of the central canal. Interestingly, Wnt expression remains in stretched roof plate cells and activates Wnt/β-catenin signaling in ependymal cells surrounding the central canal. Wnt/β-catenin signaling in ependymal cells promotes proliferation of neural progenitor and stem cells in embryonic and adult spinal cord. In this review, we focus on the role of the roof plate, especially that of Wnt ligands secreted by roof plate cells, in morphological changes occurring in the spinal cord.


Development ◽  
1998 ◽  
Vol 125 (9) ◽  
pp. 1627-1635 ◽  
Author(s):  
K. Takahashi ◽  
G.H. Nuckolls ◽  
O. Tanaka ◽  
I. Semba ◽  
I. Takahashi ◽  
...  

Distinct cranial neural crest-derived cell types (a number of neuronal as well as non-neuronal cell lineages) are generated at characteristic times and positions in the rhombomeres of the hindbrain in developing vertebrate embryos. To examine this developmental process, we developed a novel strategy designed to test the efficacy of gain-of-function Msx2 expression within rhombomeres in ovo prior to the emigration of cranial neural crest cells (CNCC). Previous studies indicate that CNCC from odd-numbered rhombomeres (r3 and r5) undergo apoptosis in response to exogenous BMP4. We provide evidence that targeted infection in ovo using adenovirus containing Msx2 and a reporter molecule indicative of translation can induce apoptosis in either even- or odd-numbered rhombomeres. Furthermore, infected lacZ-control explants indicated that CNCC emigrated, and that 20% of these cells were double positive for crest cell markers HNK-1 and beta-gal. In contrast, there were no HNK-1 and Msx2 double positive cells emigrating from Msx2 infected explants. These results support the hypothesis that apoptotic elimination of CNCC can be induced by ‘gain-of-function’ Msx2 expression in even-numbered rhombomeres. These inductive interactions involve qualitative, quantitative, positional and temporal differences in TGF-beta-related signals, Msx2 expression and other transcriptional control.


2008 ◽  
Vol 2008 (2) ◽  
pp. pdb.prot4925-pdb.prot4925 ◽  
Author(s):  
S. R. Kadison ◽  
C. E. Krull

Development ◽  
1993 ◽  
Vol 119 (1) ◽  
pp. 233-245 ◽  
Author(s):  
A. Graham ◽  
I. Heyman ◽  
A. Lumsden

Neural crest cells originate at three discontinuous levels along the rostrocaudal axis of the chick rhombencephalon, centred on rhombomeres 1 and 2, 4 and 6, respectively. These are separated by the odd-numbered rhombomeres r3 and r5 which are depleted of migratory neural crest cells. Here we show elevated levels of apoptosis in the dorsal midline of r3 and r5, immediately following the formation of these rhombomeres at the developmental stage (10–12) when neural crest cells would be expected to emerge at these neuraxial levels. These regions are also marked by their expression of members of the msx family of homeobox genes with msx-2 expression preceding apoptosis in a precisely colocalised pattern. In vitro and in ovo experiments have revealed that r3 and r5 are depleted of neural crest cells by an interaction within the neural epithelium: if isolated or distanced from their normal juxtaposition with even-numbered rhombomeres, both r3 and r5 produce migrating neural crest cells. When r3 or r5 are unconstrained in this way, allowing production of crest, msx-2 expression is concomitantly down regulated. This suggests a correlation between msx-2 and the programming of apoptosis in this system. The hindbrain neural crest is thus produced in discrete streams by mechanisms intrinsic to the neural epithelium. The crest cells that enter the underlying branchial region are organised into streams before they encounter the mesodermal environment lateral to the neural tube. This contrasts sharply with the situation in the trunk where neural crest production is uninterrupted along the neuraxis and the segmental accumulation of neurogenic crest cells is subsequently founded on an alternation of permissive and non-permissive qualities of the local mesodermal environment.


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