The migration of neural crest cells and the growth of motor axons through the rostral half of the chick somite

Development ◽  
1985 ◽  
Vol 90 (1) ◽  
pp. 437-455
Author(s):  
M. Rickmann ◽  
J. W. Fawcett ◽  
R. J. Keynes
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Critical Role ◽  
Neural Crest Cells ◽  
Ventral Root ◽  
Lateral Part ◽  
Motor Axons ◽  
Migration Pathway ◽  
Extracellular Matrix Components ◽  
Pass Through

We have studied the pathway of migration of neural crest cells through the somites of the developing chick embryo, using the monoclonal antibodies NC-1 and HNK-1 to stain them. Crest cells, as they migrate ventrally from the dorsal aspect of the neural tube, pass through the lateral part of the sclerotome, but only through that part of the sclerotome which lies in the rostral half of each somite. This migration pathway is almost identical to the path which presumptive motor axons take when they grow out from the neural tube shortly after the onset of neural crest migration. In order to see whether the ventral root axons are guided along this pathway by neural crest cells, we surgically excised the neural crest from a series of embryos, and examined the pattern of axon outgrowth approximately 24 h later. In somites which contained no neural crest cells, ventral root axons were still found only in the rostral half of the somite, although axonal growth was slightly delayed. These axons were surrounded by sheath cells, which had presumably migrated out of the neural tube, to a point about 50 μm proximal to the growth cones. With appropriate antibodies we found that the extracellular matrix components fibronectin and laminin are evenly distributed between the rostral and caudal halves of the somite. Neither of these molecules therefore plays a critical role in determining the specific pathway of neural crest cells or motor axons through the rostral half of the somite.

Axons arrest the migration of Schwann cell precursors

Development ◽  
1994 ◽  
Vol 120 (6) ◽  
pp. 1411-1420 ◽  
Author(s):  
A. Bhattacharyya ◽  
R. Brackenbury ◽  
N. Ratner
Keyword(s):  
Schwann Cell ◽  
Motor Neuron ◽  
Neural Crest ◽  
Schwann Cells ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Ventral Root ◽  
Motor Axons ◽  
Ventral Neural Tube ◽  
Schwann Cell Precursors

The neural crest gives rise to a variety of cell types including Schwann cells of the peripheral nervous system. Schwann cell precursors begin to differentiate early and migrate along specific pathways in the embryo before associating with nerve trunks. To determine whether motor axons direct the migration of Schwann cell precursors along specific pathways, we tested the effect of ablating the ventral half of the neural tube, which contains motor neuron cell bodies. The ventral neural tube was removed unilaterally from lumbar regions of chicken embryos at stage 17, when neural crest cells are just beginning to migrate and before motor axons have extended out of the neural tube. At several stages after ventral tube ablation, sections of the lumbar region of these embryos were stained with anti-acetylated tubulin to label developing axons, HNK-1 to label migrating neural crest cells and 1E8 to label Schwann cell precursors. In many embryos the ablation of motor neurons was incomplete. The staining patterns in these embryos support the idea that some Schwann cells are derived from the neural tube. In embryos with complete motor neuron ablation, at stage 18, HNK-1-positive neural crest cells had migrated to normal locations in both control and ablated sides of the embryo, suggesting that motor axons or the ventral neural tube are not required for proper migration of neural crest cells. However, by stage 19, cells that were positive for HNK-1 or 1E8 were no longer seen in the region of the ventral root, nor ventral to the ventral root region. Because Schwann cell precursors require neural-derived factors for their survival in vitro, we tested whether neural crest cells that migrate to the region of the ventral root in ventral neural tube-ablated embryos then die. Nile Blue staining for dead and dying cells in ventral neural tube-ablated embryos provided no evidence for cell death at stage 18. These results suggest that motor axons arrest the migration of Schwann cell precursors during neural crest migration.

scholarly journals Tissue interactions affecting the migration and differentiation of neural crest cells in the chick embryo

Development ◽  
1991 ◽  
Vol 113 (1) ◽  
pp. 207-216 ◽  
Author(s):  
C.D. Stern ◽  
K.B. Artinger ◽  
M. Bronner-Fraser
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Dorsal Root ◽  
Ganglion Cells ◽  
Neural Crest Cells ◽  
Motor Axons ◽  
Root Region ◽  
Tissue Interactions ◽  
Catecholamine Fluorescence ◽  
Catecholaminergic Cells

A series of microsurgical operations was performed in chick embryos to study the factors that control the polarity, position and differentiation of the sympathetic and dorsal root ganglion cells developing from the neural crest. The neural tube, with or without the notochord, was rotated by 180 degrees dorsoventrally to cause the neural crest cells to emerge ventrally. In some embryos, the notochord was ablated, and in others a second notochord was implanted. Sympathetic differentiation was assessed by catecholamine fluorescence after aldehyde fixation. Neural crest cells emerging from an inverted neural tube migrate in a ventral-to-dorsal direction through the sclerotome, where they become segmented by being restricted to the rostral half of each sclerotome. Both motor axons and neural crest cells avoid the notochord and the extracellular matrix that surrounds it, but motor axons appear also to be attracted to the notochord until they reach its immediate vicinity. The dorsal root ganglia always form adjacent to the neural tube and their dorsoventral orientation follows the direction of migration of the neural crest cells. Differentiation of catecholaminergic cells only occurs near the aorta/mesonephros and in addition requires the proximity of either the ventral neural tube (floor plate/ventral root region) or the notochord. Prior migration of presumptive catecholaminergic cells through the sclerotome, however, is neither required nor sufficient for their adrenergic differentiation.

Neural crest emigration from the neural tube depends on regulated cadherin expression

Development ◽  
1998 ◽  
Vol 125 (15) ◽  
pp. 2963-2971 ◽  
Author(s):  
S. Nakagawa ◽  
M. Takeichi
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Critical Role ◽  
Neural Crest Cells ◽  
Migration Pattern ◽  
Dominant Negative ◽  
Expression Vectors ◽  
Neural Tubes ◽  
Neuroepithelial Cells

During the emergence of neural crest cells from the neural tube, the expression of cadherins dynamically changes. In the chicken embryo, the early neural tube expresses two cadherins, N-cadherin and cadherin-6B (cad6B), in the dorsal-most region where neural crest cells are generated. The expression of these two cadherins is, however, downregulated in the neural crest cells migrating from the neural tube; they instead begin expressing cadherin-7 (cad7). As an attempt to investigate the role of these changes in cadherin expression, we overexpressed various cadherin constructs, including N-cadherin, cad7, and a dominant negative N-cadherin (cN390), in neural crest-generating cells. This was achieved by injecting adenoviral expression vectors encoding these molecules into the lumen of the closing neural tube of chicken embryos at stage 14. In neural tubes injected with the viruses, efficient infection was observed at the neural crest-forming area, resulting in the ectopic cadherin expression also in migrating neural crest cells. Notably, the distribution of neural crest cells with the ectopic cadherins changed depending on which constructs were expressed. Many crest cells failed to escape from the neural tube when N-cadherin or cad7 was overexpressed. Moreover, none of the cells with these ectopic cadherins migrated along the dorsolateral (melanocyte) pathway. When these samples were stained for Mitf, an early melanocyte marker, positive cells were found accumulated within the neural tube, suggesting that the failure of their migration was not due to differentiation defects. In contrast to these phenomena, cells expressing non-functional cadherins exhibited a normal migration pattern. Thus, the overexpression of a neuroepithelial cadherin (N-cadherin) and a crest cadherin (cad7) resulted in the same blocking effect on neural crest segregation from neuroepithelial cells, especially for melanocyte precursors. These findings suggest that the regulation of cadherin expression or its activity at the neural crest-forming area plays a critical role in neural crest emigration from the neural tube.

The neural tube origin of ventral root sheath cells in the chick embryo

Development ◽  
1987 ◽  
Vol 101 (2) ◽  
pp. 247-254 ◽  
Author(s):  
E.R. Lunn ◽  
J. Scourfield ◽  
R.J. Keynes ◽  
C.D. Stern
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Ventral Root ◽  
Phenotypic Traits ◽  
Motor Axons ◽  
Root Cells ◽  
Root Exit Zone ◽  
Root Sheath ◽  
Embryonic Origin ◽  
Sheath Cells

The embryonic origin of peripheral nerve Schwann/sheath cells is still uncertain. Although the neural crest is known to be an important source, it is not clear whether the ventral neural tube also contributes a progenitor population for motor axons. We have used the techniques of immunohistochemistry, electron microscopy and quail-chick grafting to examine this problem. Immunohistochemistry with monoclonal antibody HNK-1 identified a cluster of immunoreactive cells in the sclerotome, at the site of the future ventral root. With the electron microscope, nucleated cells could not be seen breaching the basal lamina of the neural tube, exclusively in the region of the ventral root and preceding axon outgrowth. After grafting a length of crest-ablated quail neural tube in place of host chick neural tube, a population of quail cells was found localized to the ventral root exit zone, associated with the ventral root axons. Taken together, these observations support the possibility of a neural tube origin for ventral root sheath cells, although we found no evidence for a more extensive migration of these cells. The ventral root cells share certain phenotypic traits, such as HNK-1 immunoreactivity, with neural-crest-derived Schwann cells, but are not necessarily identical to them. We argue that while they may help motor axons to exit the neural tube at the correct position, they are unlikely to guide axons beyond the immediate vicinity of the neural tube.

Changes in the distribution of extracellular matrix components during neural crest development in Xiphophorus spp. embryos

1994 ◽  
Vol 72 (7) ◽  
pp. 1340-1353 ◽  
Author(s):  
Bahram Sadaghiani ◽  
Bruce J. Crawford ◽  
Juergen R. Vielkind
Keyword(s):  
Extracellular Matrix ◽  
Neural Crest ◽  
Critical Role ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Weak Staining ◽  
Extracellular Matrix Components ◽  
Neural Crest Cell Migration ◽  
And Migration ◽  
Migration Pathways

The changes in distribution of chondroitin sulfate proteoglycans (CSs) and fibronectin (FN), two major components of the extracellular matrix (ECM), are described during the development and migration of neural crest cells in two Xiphophorus species offish, X. helleri (swordtail) and X. maculatus (platyfish), using immunohistochemistry. A detailed description of the developmental changes in HNK-1-positive ECM components is also provided and compared with those of CSs and FN. HNK-1 antigen was also used as a marker for the neural crest cells. Weak staining for CSs, FN, and HNK-1-positive ECM was present in the neural crest cell migration pathways prior to migration of the cells. The level of staining increased dramatically during migration of these cells and decreased again after migration was nearly completed. Staining for CSs was more widespread than staining for FN, while the HNK-1 staining pattern was more clearly restricted to the migratory pathways than those seen with the other two antibodies. The correlation between the spatiotemporal relationship of these ECM components and the segregation and migration of neural crest cells suggests that these ECM molecules may be involved in both initiating and guiding the migration of neural crest cells in these fish. The HNK-1-positive ECM may play a more critical role than CSs and FN.

Induction of melanocyte precursors from neural crest cells surrounding the neural tube-like structures developed in vitro using mouse ES cell culture

2007 ◽  
Vol 27 (1) ◽  
pp. 45-52
Author(s):  
Koh-ichi Atoh ◽  
Manae S. Kurokawa ◽  
Hideshi Yoshikawa ◽  
Chieko Masuda ◽  
Erika Takada ◽  
...  
Keyword(s):  
Cell Culture ◽  
Neural Crest ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Es Cell ◽  
Mouse Es Cell

An experimental study on neural crest migration in Barbus conchonius (Cyprinidae, Teleostei), with special reference to the origin of the enteroendocrine cells

Development ◽  
1981 ◽  
Vol 62 (1) ◽  
pp. 309-323
Author(s):  
C. H. J. Lamers ◽  
J. W. H. M. Rombout ◽  
L. P. M. Timmermans
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Ganglion Cells ◽  
Neural Crest Cells ◽  
Enteroendocrine Cells ◽  
Pigment Cells ◽  
Transplantation Technique ◽  
Spinal Ganglion Cells ◽  
Neural Crest Origin ◽  
Neural Crest Migration

A neural crest transplantation technique is described for fish. As in other classes ofvertebrates, two pathways of neural crest migration can be distinguished: a lateroventral pathway between somites and ectoderm, and a medioventral pathway between somites and neural tube/notochord. In this paper evidence is presented for a neural crest origin of spinal ganglion cells and pigment cells, and indication for such an origin is obtained for sympathetic and enteric ganglion cells and for cells that are probably homologues to adrenomedullary and paraganglion cells in the future kidney area. The destiny of neural crest cells near the developing lateral-line sense organs is discussed. When grafted into the yolk, neural crest cells or neural tube cells appear to differentiate into ‘periblast cells’; this suggests a highly activating influence of the yolk. Many neural crest cells are found around the urinary ducts and, when grafted below the notochord, even within the urinary duct epithelium. These neural crest cells do not invade the gut epithelium, even when grafted adjacent to the developing gut. Consequently enteroendocrine cells in fish are not likely to have a trunkor rhombencephalic neural crest origin. Another possible origin of these cells will be proposed.

scholarly journals Bimodal function of chromatin remodeler Hmga1 in neural crest induction and Wnt-dependent emigration

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Shashank Gandhi ◽  
Erica J Hutchins ◽  
Krystyna Maruszko ◽  
Jong H Park ◽  
Matthew Thomson ◽  
...  
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Neural Plate ◽  
Chromatin Remodeler ◽  
Lineage Specification ◽  
Dorsal Neural Tube ◽  
Neural Crest Development ◽  
Neural Plate Border ◽  
Canonical Wnt

During gastrulation, neural crest cells are specified at the neural plate border, as characterized by Pax7 expression. Using single-cell RNA sequencing coupled with high-resolution in situ hybridization to identify novel transcriptional regulators, we show that chromatin remodeler Hmga1 is highly expressed prior to specification and maintained in migrating chick neural crest cells. Temporally controlled CRISPR-Cas9-mediated knockouts uncovered two distinct functions of Hmga1 in neural crest development. At the neural plate border, Hmga1 regulates Pax7-dependent neural crest lineage specification. At premigratory stages, a second role manifests where Hmga1 loss reduces cranial crest emigration from the dorsal neural tube independent of Pax7. Interestingly, this is rescued by stabilized ß-catenin, thus implicating Hmga1 as a canonical Wnt activator. Together, our results show that Hmga1 functions in a bimodal manner during neural crest development to regulate specification at the neural plate border, and subsequent emigration from the neural tube via canonical Wnt signaling.

scholarly journals A vital dye analysis of the timing and pathways of avian trunk neural crest cell migration

Development ◽  
1989 ◽  
Vol 106 (4) ◽  
pp. 809-816 ◽  
Author(s):  
G.N. Serbedzija ◽  
M. Bronner-Fraser ◽  
S.E. Fraser
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Sympathetic Ganglia ◽  
Pigment Cells ◽  
Root Cells ◽  
Vital Dye ◽  
Rostral Portion ◽  
Crest Cell

To permit a more detailed analysis of neural crest cell migratory pathways in the chick embryo, neural crest cells were labelled with a nondeleterious membrane intercalating vital dye, DiI. All neural tube cells with endfeet in contact with the lumen, including premigratory neural crest cells, were labelled by pressure injecting a solution of DiI into the lumen of the neural tube. When assayed one to three days later, migrating neural crest cells, motor axons, and ventral root cells were the only cells types external to the neural tube labelled with DiI. During the neural crest cell migratory phase, distinctly labelled cells were found along: (1) a dorsolateral pathway, under the epidermis, as well adjacent to and intercalating through the dermamyotome; and (2) a ventral pathway, through the rostral portion of each sclerotome and around the dorsal aorta as described previously. In contrast to those cells migrating through the sclerotome, labelled cells on the dorsolateral pathway were not segmentally arranged along the rostrocaudal axis. DiI-labelled cells were observed in all truncal neural crest derivatives, including subepidermal presumptive pigment cells, dorsal root ganglia, and sympathetic ganglia. By varying the stage at which the injection was performed, neural crest cell emigration at the level of the wing bud was shown to occur from stage 13 through stage 22. In addition, neural crest cells were found to populate their derivatives in a ventral-to-dorsal order, with the latest emigrating cells migrating exclusively along the dorsolateral pathway.

Pax3 is required for cardiac neural crest migration in the mouse: evidence from the splotch (Sp2H) mutant

Development ◽  
1997 ◽  
Vol 124 (2) ◽  
pp. 505-514 ◽  
Author(s):  
S.J. Conway ◽  
D.J. Henderson ◽  
A.J. Copp
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Outflow Tract ◽  
Avian Embryo ◽  
Cardiac Neural Crest ◽  
Branchial Arches ◽  
Aortic Arches ◽  
Cardiac Outflow

Neural crest cells originating in the occipital region of the avian embryo are known to play a vital role in formation of the septum of the cardiac outflow tract and to contribute cells to the aortic arches, thymus, thyroid and parathyroids. This ‘cardiac’ neural crest sub-population is assumed to exist in mammals, but without direct evidence. In this paper we demonstrate, using RT-PCR and in situ hybridisation, that Pax3 expression can serve as a marker of cardiac neural crest cells in the mouse embryo. Cells of this lineage were traced from the occipital neural tube, via branchial arches 3, 4 and 6, into the aortic sac and aorto-pulmonary outflow tract. Confirmation that these Pax3-positive cells are indeed cardiac neural crest is provided by experiments in which hearts were deprived of a source of colonising neural crest, by organ culture in vitro, with consequent lack of up-regulation of Pax3. Occipital neural crest cell outgrowths in vitro were also shown to express Pax3. Mutation of Pax3, as occurs in the splotch (Sp2H) mouse, results in development of conotruncal heart defects including persistent truncus arteriosus. Homozygotes also exhibit defects of the aortic arches, thymus, thyroid and parathyroids. Pax3-positive neural crest cells were found to emigrate from the occipital neural tube of Sp2H/Sp2H embryos in a relatively normal fashion, but there was a marked deficiency or absence of neural crest cells traversing branchial arches 3, 4 and 6, and entering the cardiac outflow tract. This decreased expression of Pax3 in Sp2H/Sp2H embryos was not due to down-regulation of Pax3 in neural crest cells, as use of independent neural crest markers, Hoxa-3, CrabpI, Prx1, Prx2 and c-met also revealed a deficiency of migrating cardiac neural crest cells in homozygous embryos. This work demonstrates the essential role of the cardiac neural crest in formation of the heart and great vessels in the mouse and, furthermore, shows that Pax3 function is required for the cardiac neural crest to complete its migration to the developing heart.

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