scholarly journals Early Migrating Neural Crest Cells Can Form Ventral Neural Tube Derivatives When Challenged by Transplantation

1998 ◽  
Vol 203 (2) ◽  
pp. 295-304 ◽  
Author(s):  
Seth Ruffins ◽  
Kristin Bruk Artinger ◽  
Marianne Bronner-Fraser
Development ◽  
1996 ◽  
Vol 122 (11) ◽  
pp. 3393-3407 ◽  
Author(s):  
G. Couly ◽  
A. Grapin-Botton ◽  
P. Coltey ◽  
N.M. Le Douarin

The mesencephalic and rhombencephalic levels of origin of the hypobranchial skeleton (lower jaw and hyoid bone) within the neural fold have been determined at the 5-somite stage with a resolution corresponding to each single rhombomere, by means of the quail-chick chimera technique. Expression of certain Hox genes (Hoxa-2, Hoxa-3 and Hoxb-4) was recorded in the branchial arches of chick and quail embryos at embryonic days 3 (E3) and E4. This was a prerequisite for studying the regeneration capacities of the neural crest, after the dorsal neural tube was resected at the mesencephalic and rhombencephalic level. We found first that excisions at the 5-somite stage extending from the midmesencephalon down to r8 are followed by the regeneration of neural crest cells able to compensate for the deficiencies so produced. This confirmed the results of previous authors who made similar excisions at comparable (or older) developmental stages. When a bilateral excision was followed by the unilateral homotopic graft of the dorsal neural tube from a quail embryo, thus mimicking the situation created by a unilateral excision, we found that the migration of the grafted unilateral neural crest (quail-labelled) is bilateral and compensates massively for the missing crest derivatives. The capacity of the intermediate and ventral neural tube to yield neural crest cells was tested by removing the chick rhombencephalic neural tube and replacing it either uni- or bilaterally with a ventral tube coming from a stage-matched quail. No neural crest cells exited from the ventral neural tube but no deficiency in neural crest derivatives was recorded. Crest cells were found to regenerate from the ends of the operated region. This was demonstrated by grafting fragments of quail neural fold at the extremities of the excised territory. Quail neural crest cells were seen migrating longitudinally from both the rostral and caudal ends of the operated region and filling the branchial arches located inbetween. Comparison of the behaviour of neural crest cells in this experimental situation with that showed by their normal fate map revealed that crest cells increase their proliferation rate and change their migratory behaviour without modifying their Hox code.


Development ◽  
1993 ◽  
Vol 118 (4) ◽  
pp. 1049-1062 ◽  
Author(s):  
T. Scherson ◽  
G. Serbedzija ◽  
S. Fraser ◽  
M. Bronner-Fraser

In avian embryos, cranial neural crest cells emigrate from the dorsal midline of the neural tube shortly after neural tube closure. Previous lineage analyses suggest that the neural crest is not a pre-segregated population of cells within the neural tube; instead, a single progenitor in the dorsal neural tube can contribute to neurons in both the central and the peripheral nervous systems (Bronner-Fraser and Fraser, 1989 Neuron 3, 755–766). To explore the relationship between the ‘premigratory’ neural crest cells and the balance of the cells in the neural tube in the midbrain and hindbrain region, we have challenged the fate of these populations by ablating the neural crest either alone or in combination with the adjoining ventral portions of the neural tube. Focal injections of the vital dye, DiI, into the neural tissue bordering the ablated region demonstrate that cells at the same axial level, in the lateral and ventral neural tube, regulate to reconstitute a population of neural crest cells. These cells emigrate from the neural tube, migrate along normal pathways according to their axial level of origin and appear to give rise to a normal range of derivatives. This regulation following ablation suggests that neural tube cells normally destined to form CNS derivatives can adjust their prospective fates to form PNS and other neural crest derivatives until 4.5-6 hours after the time of normal onset of emigration from the neural tube.


Development ◽  
1994 ◽  
Vol 120 (6) ◽  
pp. 1411-1420 ◽  
Author(s):  
A. Bhattacharyya ◽  
R. Brackenbury ◽  
N. Ratner

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.


Development ◽  
1996 ◽  
Vol 122 (1) ◽  
pp. 231-241 ◽  
Author(s):  
M.S. Spence ◽  
J. Yip ◽  
C.A. Erickson

Somites, like all axial structures, display dorsoventral polarity. The dorsal portion of the somite forms the dermamyotome, which gives rise to the dermis and axial musculature, whereas the ventromedial somite disperses to generate the sclerotome, which later comprises the vertebrae and intervertebral discs. Although the neural tube and notochord are known to regulate some aspects of this dorsoventral pattern, the precise tissues that initially specify the dermamyotome, and later the myotome from it, have been controversial. Indeed, dorsal and ventral neural tube, notochord, ectoderm and neural crest cells have all been proposed to influence dermamyotome formation or to regulate myocyte differentiation. In this report we describe a series of experimental manipulations in the chick embryo to show that dermamyotome formation is regulated by interactions with the dorsal neural tube. First, we demonstrate that when a neural tube is rotated 180 degrees around its dorsoventral axis, a secondary dermamyotome is induced from what would normally have developed as sclerotome. Second, if we ablate the dorsal neural tube, dermamyotomes are absent in the majority of embryos. Third, if we graft pieces of dorsal neural tube into a ventral position between the notochord and ventral somite, a dermamyotome develops from the sclerotome that is proximate to the graft, and myocytes differentiate. In addition, we also show that myogenesis can be regulated by the dorsal neural tube because when pieces of dorsal neural tube and unsegmented paraxial mesoderm are combined in tissue culture, myocytes differentiate, whereas mesoderm cultures alone do not produce myocytes autonomously. In all of the experimental perturbations in vivo, the dorsal neural tube induced dorsal structures from the mesoderm in the presence of notochord and floorplate, which have been reported previously to induce sclerotome. Thus, we have demonstrated that in the context of the embryonic environment, a dorsalizing signal from the dorsal neural tube can compete with the diffusible ventralizing signal from the notochord. In contrast to dorsal neural tube, pieces of ventral neural tube, dorsal ectoderm or neural crest cells, all of which have been postulated to control dermamyotome formation or to induce myogenesis, either fail to do so or provoke only minimal inductive responses in any of our assays. However, complicating the issue, we find consistent with previous studies that following ablation of the entire neural tube, dermamyotome formation still proceeds adjacent to the dorsal ectoderm. Together these results suggest that, although dorsal ectoderm may be less potent than the dorsal neural tube in inducing dermamyotome, it does nonetheless possess some dermamyotomal-inducing activity. Based on our data and that of others, we propose a model for somite dorsoventral patterning in which competing diffusible signals from the dorsal neural tube and from the notochord/floorplate specify dermamyotome and sclerotome, respectively. In our model, the positioning of the dermamyotome dorsally is due to the absence or reduced levels of the notochord-derived ventralizing signals, as well as to the presence of dominant dorsalizing signals. These dorsal signals are possibly localized and amplified by binding to the basal lamina of the ectoderm, where they can signal the underlying somite, and may also be produced by the ectoderm as well.


2007 ◽  
Vol 27 (1) ◽  
pp. 45-52
Author(s):  
Koh-ichi Atoh ◽  
Manae S. Kurokawa ◽  
Hideshi Yoshikawa ◽  
Chieko Masuda ◽  
Erika Takada ◽  
...  

Development ◽  
1981 ◽  
Vol 62 (1) ◽  
pp. 309-323
Author(s):  
C. H. J. Lamers ◽  
J. W. H. M. Rombout ◽  
L. P. M. Timmermans

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.


eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Shashank Gandhi ◽  
Erica J Hutchins ◽  
Krystyna Maruszko ◽  
Jong H Park ◽  
Matthew Thomson ◽  
...  

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.


Development ◽  
1989 ◽  
Vol 106 (4) ◽  
pp. 809-816 ◽  
Author(s):  
G.N. Serbedzija ◽  
M. Bronner-Fraser ◽  
S.E. Fraser

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.


Development ◽  
1997 ◽  
Vol 124 (2) ◽  
pp. 505-514 ◽  
Author(s):  
S.J. Conway ◽  
D.J. Henderson ◽  
A.J. Copp

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.


Development ◽  
1983 ◽  
Vol 74 (1) ◽  
pp. 97-118
Author(s):  
C. A. Erickson ◽  
J. A. Weston

The cellular morphology and migratory pathways of the trunk neural crest are described in normal mouse embryos, and in embryos homozygous for Patch in which neural crest derivatives develop abnormally. Trunk neural crest cells initially appear in 8½-day embryos as a unique cell population on the dorsal neural tube surface and are relatively rounded. Once they begin to migrate the cells flatten and orient somewhat tangentially to the neural tube, and advance ventrad between the somites and neural tube. At the onset of migration neural crest cells extend lamellipodia onto the surface of the tube while detaching their trailing processes from the lumenal surface. The basal lamina on the dorsal neural tube is discontinuous when cell migration begins in this region. As development proceeds, the basal lamina gradually becomes continuous from a lateral to dorsal direction and neural crest emigration is progressively confined to the narrowing region of discontinuous basal lamina. Cell separation from the neural tube ceases concomitant with completion of a continuous basement membrane. Preliminary observations of the mutant embryos reveal that abnormal extracellular spaces appear and patterns of crest migration are subsequently altered. We conclude that the extracellular matrix, extracellular spaces and basement membranes may delimit crest migration in the mouse.


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