THE DETERMINATION OF THE AUDITORY PLACODE IN THE CHICK

1. The presumptive ear ectoderm, removed from its normal site and transplanted to the amnio-cardiac vesicle, does not develop into an otic placode unless it comes from an embryo with more than nine pairs of somites. 2. The ectoderm which grows over the place from which the presumptive ear ectoderm is removed is induced to form an otic placode, the size of the placode being smaller the older the embryo at the time of operation. 3. If the wall of the neural tube, including the neural crest, is removed from the region of the ear in embryos younger than the nine-somite stage, an ear may nevertheless be formed. Since the ear ectoderm at this stage is not capable of differentiating when isolated, this result shows that inducing agencies other than the neural material are active at this stage. In some of the operated embryos, the acoustico-facialis ganglion was completely lacking, so this structure cannot be the sole organizer of the ear, as Szepsenwol suggested. 4. If both the wall of the neural tube and the presumptive ear ectoderm are removed, no ear is formed even in stages younger than the nine-somite stage, so that it appears that the non-neural inducing agents are more effective when working on presumptive ectoderm of this age than when working on non-presumptive ectoderm. This suggests that the ear ectoderm is beginning to be determined some time before it acquires the capacity for independent differentiation. 5. The wall of the neural tube, from the ear region, can induce a small ear when grafted under the ectoderm of the anterior part of the head. 6. The evidence suggests that the induction of the ear in normal development is due to the combined action of several structures, of which the wall of the neural tube, and the tissues derived from it (ganglia), is one but not the only one.

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Neural tube-ectoderm interactions are required for trigeminal placode formation

Development ◽

10.1242/dev.124.21.4287 ◽

1997 ◽

Vol 124 (21) ◽

pp. 4287-4295 ◽

Cited By ~ 7

Author(s):

M.R. Stark ◽

J. Sechrist ◽

M. Bronner-Fraser ◽

C. Marcelle

Keyword(s):

Neural Crest ◽

Trigeminal Ganglion ◽

Neural Tube ◽

Neural Crest Cells ◽

Surface Ectoderm ◽

Somite Stage ◽

Tissue Interactions ◽

Cranial Neural Crest Cells ◽

Cranial Sensory Ganglia ◽

Placode Formation

Cranial sensory ganglia in vertebrates develop from the ectodermal placodes, the neural crest, or both. Although much is known about the neural crest contribution to cranial ganglia, relatively little is known about how placode cells form, invaginate and migrate to their targets. Here, we identify Pax-3 as a molecular marker for placode cells that contribute to the ophthalmic branch of the trigeminal ganglion and use it, in conjunction with DiI labeling of the surface ectoderm, to analyze some of the mechanisms underlying placode development. Pax-3 expression in the ophthalmic placode is observed as early as the 4-somite stage in a narrow band of ectoderm contiguous to the midbrain neural folds. Its expression broadens to a patch of ectoderm adjacent to the midbrain and the rostral hindbrain at the 8- to 10-somite stage. Invagination of the first Pax-3-positive cells begins at the 13-somite stage. Placodal invagination continues through the 35-somite stage, by which time condensation of the trigeminal ganglion has begun. To challenge the normal tissue interactions leading to placode formation, we ablated the cranial neural crest cells or implanted barriers between the neural tube and the ectoderm. Our results demonstrate that, although the presence of neural crest cells is not mandatory for Pax-3 expression in the forming placode, a diffusible signal from the neuroectoderm is required for induction and/or maintenance of the ophthalmic placode.

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The regeneration of the cephalic neural crest, a problem revisited: the regenerating cells originate from the contralateral or from the anterior and posterior neural fold

Development ◽

10.1242/dev.122.11.3393 ◽

1996 ◽

Vol 122 (11) ◽

pp. 3393-3407 ◽

Cited By ~ 31

Author(s):

G. Couly ◽

A. Grapin-Botton ◽

P. Coltey ◽

N.M. Le Douarin

Keyword(s):

Neural Crest ◽

Neural Tube ◽

Hox Genes ◽

Experimental Situation ◽

Neural Crest Cells ◽

Fate Map ◽

Somite Stage ◽

Dorsal Neural Tube ◽

Ventral Neural Tube ◽

Branchial Arches

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.

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Dorsal hindbrain ablation results in rerouting of neural crest migration and changes in gene expression, but normal hyoid development

Development ◽

10.1242/dev.124.14.2729 ◽

1997 ◽

Vol 124 (14) ◽

pp. 2729-2739 ◽

Cited By ~ 7

Author(s):

J.R. Saldivar ◽

J.W. Sechrist ◽

C.E. Krull ◽

S. Ruffins ◽

M. Bronner-Fraser

Keyword(s):

Gene Expression ◽

Neural Crest ◽

Neural Tube ◽

Neural Crest Cells ◽

Branchial Arch ◽

Surgical Ablation ◽

The Third ◽

Somite Stage ◽

Or Gene ◽

Dorsal Hindbrain

Our previous studies have shown that hindbrain neural tube cells can regulate to form neural crest cells for a limited time after neural fold removal (Scherson, T., Serbedzija, G., Fraser, S. E. and Bronner-Fraser, M. (1993). Development 188, 1049–1061; Sechrist, J., Nieto, M. A., Zamanian, R. T. and Bronner-Fraser, M. (1995). Development 121, 4103–4115). In the present study, we ablated the dorsal hindbrain at later stages to examine possible alterations in migratory behavior and/or gene expression in neural crest populations rostral and caudal to the operated region. The results were compared with those obtained by misdirecting neural crest cells via rhombomere rotation. Following surgical ablation of dorsal r5 and r6 prior to the 10 somite stage, r4 neural crest cells migrate along normal pathways toward the second branchial arch. Similarly, r7 neural crest cells migrate primarily to the fourth branchial arch. When analogous ablations are performed at the 10–12 somite stage, however, a marked increase in the numbers of DiI/Hoxa-3-positive cells from r7 are observed within the third branchial arch. In addition, some DiI-labeled r4 cells migrate into the depleted hindbrain region and the third branchial arch. During their migration, a subset of these r4 cells up-regulate Hoxa-3, a transcript they do not normally express. Krox20 transcript levels were augmented after ablation in a population of neural crest cells migrating from r4, caudal r3 and rostral r3. Long-term survivors of bilateral ablations possess normal neural crest-derived cartilage of the hyoid complex, suggesting that misrouted r4 and r7 cells contribute to cranial derivatives appropriate for their new location. In contrast, misdirecting of the neural crest by rostrocaudal rotation of r4 through r6 results in a reduction of Hoxa-3 expression in the third branchial arch and corresponding deficits in third arch-derived structures of the hyoid apparatus. These results demonstrate that neural crest/tube progenitors in the hindbrain can compensate by altering migratory trajectories and patterns of gene expression when the adjacent neural crest is removed, but fail to compensate appropriately when the existing neural crest is misrouted by neural tube rotation.

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Abnormal neural fold development in trisomy 12 and trisomy 14 mouse embryos

Development ◽

10.1242/dev.66.1.141 ◽

1981 ◽

Vol 66 (1) ◽

pp. 141-158

Author(s):

Barbara Putz ◽

Gillian Morriss-Kay

Keyword(s):

Neural Tube ◽

Anterior Part ◽

Tube Formation ◽

Mouse Embryos ◽

Somite Stage ◽

Mammalian Embryos ◽

Trisomy 12 ◽

Optic Vesicles ◽

Normal Laboratory ◽

Neural Tube Formation

The early development of the exencephalic malformation in trisomy 12 (Tsl2) and trisomy 14 (Tsl4) mouse embryos was examined by means of scanning electron microscopy and compared with cranial neural tube formation in euploid litter-mates. Embryos from normal laboratory mice were used as additional controls. The euploid control embryos of the trisomy-inducing breeding system showed a slight delay and some variation in the timing of cranial neurulation. The pre-exencephalic trisomic embryos showed hypoplasia, and lower somite number when compared with euploid littermates; there was also a retardation of development of the whole neural tube, when related to the somite stage. External differences from the control embryos were observed at the late pre-somite stage, when the anterior part of the neural plate showed a crumpled appearance. At 6 somites the lateral edges of the forebrain were everted instead of elevated in Tsl2 and Tsl4 embryos. At later stages, however, the forebrain showed a tendency towards the normal morphogenetic pattern, so that the optic vesicles were eventually formed and the most anterior part fused. The caudal forebrain and the midbrain were more permanently affected by the disturbance of trisomic conditions and grew laterally, failing to appose or fuse in the midline in both Tsl2 and Tsl4 embryos. Hindbrain morphogenesis was different in Tsl2 and Tsl4 excencephaly: in Tsl2 embryos it did not close rostral to the otic pits, whereas in Tsl4 embryos it showed a normal closure up to the hindbrain/midbrain junction. These observations support the hypothesis that in mammalian embryos the mechanism of neural tube formation of the future brain region is more complex than that of the spinal neural tube and therefore may be more likely to react to a general delay of neurulation with a gross malformation. Tsl2 and Tsl4 exencephaly are due to a primary non-closure of the neural tube.

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Sox2 gene regulation via the D1 enhancer in embryonic neural tube and neural crest by the combined action of SOX2 and ZIC2

Genes to Cells ◽

10.1111/gtc.12753 ◽

2020 ◽

Vol 25 (4) ◽

pp. 242-256 ◽

Cited By ~ 2

Author(s):

Hideaki Iida ◽

Yoko Furukawa ◽

Machiko Teramoto ◽

Hitomi Suzuki ◽

Tatsuya Takemoto ◽

...

Keyword(s):

Gene Regulation ◽

Neural Crest ◽

Neural Tube ◽

Sox2 Gene ◽

Combined Action

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The Effect of Stress and Warfarin on the Adrenal Gland in Relation to Spontaneous Hemorrhage, as Judged by Measurement of Adrenal Ascorbic Acid and Serum Corticosterone

Thrombosis and Haemostasis ◽

10.1055/s-0038-1653675 ◽

1971 ◽

Vol 26 (02) ◽

pp. 275-288 ◽

Cited By ~ 3

Author(s):

S Chattopadhyay ◽

D. D Johnson ◽

G. J Millar ◽

L. B Jaques

Keyword(s):

Ascorbic Acid ◽

Acid Concentration ◽

Ascorbic Acid Concentration ◽

Corticosterone Concentration ◽

Serum Corticosterone ◽

Spontaneous Hemorrhage ◽

Combined Action ◽

Series Of Experiments ◽

Pituitary Adrenal Axis

SummaryRats were subjected to the following procedures: No treatment, Stressor (10% NaCl i.p.), Warfarin for 7 days, Stressor followed by Warfarin; and groups were sacrificed at intervals for assessment of spontaneous hemorrhage and of adrenal ascorbic acid concentration. There was no hemorrhage in the no treatment and stressor groups; some hemorrhage in the warfarin group; profound hemorrhage with Warfarin + Stressor. The adrenal ascorbic acid concentration was found to be lower, 8 h and again 5 days after stress, and remained lower in the warfarin + stress animals. Warfarin had no effect on adrenal ascorbic acid level.In another series of experiments in which the stress consisted of an electric current to the cage floor for 6 sec over 15 min, rats were sacrificed daily for determination of serum corticosterone concentration and occurrence of spontaneous hemorrhage. There was a statistically significant increase of serum corticosterone concentration with stress, warfarin and combined warfarin and stress treatments (P< 0.001 for all three variables). There was a significant correlation (r = 0.96 and 0.89, P< 0.01) for serum corticosterone concentration with hemorrhage score and incidence of hemorrhage in stressed rats receiving warfarin, but not in those receiving only warfarin. The results indicate an activation, rather than an exhaustion, of the pituitary-adrenal axis during the combined action of anticoagulant and stress, which results in the development of spontaneous hemorrhage.

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