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At least 469 records · Page 26Linked to original sources
PubMed1998

Segmentation, crest prespecification and the control of facial form.

The early development of the vertebrate head is dependent on the formation of two series of segmented structures, the rhombomeres of the hindbrain and the branchial arch series. The initial formation of these two systems is closely linked, as the principal source of branchial arch mesenchyme is the neural crest, which derives from the lateral edge of the neural plate at the time of rhombomere formation. The subsequent development of the two systems maintains a close level of integration, as specific spatial relationships between skeletal, muscle and neural elements arising from the same axial level are established. Given the level of conservation of these anatomical relationships in vertebrates, it is likely that they are a reflection of a key mechanism in early facial and pharyngeal development. One model, in part based on these findings, proposed that the neural crest acquires an axial-level specific combination of gene expression while part of the neural plate. This prepattern is then maintained throughout the crest's subsequent development. In the model, this combination of gene expression would then specify the form of the facial and pharyngeal structures that the crest would give rise to. In this review we evaluate recent evidence on whether early facial development involves a crest prespecification of this type, and conclude that it is not the case.

Animals↗
PubMed2006

Cloning and embryonic expression of five distinct sfrp genes in the zebrafish Danio rerio.

Recently, a new member of the secreted frizzled-related protein (sFRP) family, named tlc, has been identified as expressed by the anterior neural border (ANB) cells in the zebrafish Danio rerio. Tlc plays an important role in telencephalic induction and patterning. In absence of Tlc, formation of the telencephalon is severely delayed, but not abolished. This prompted us to clone the other zebrafish sfrp family members and analyse their expression patterns, in search of a family member that may partly functionally overlap with Tlc. Except sizzled, expression profile of sfrp genes in zebrafish has not been reported so far. Here, we describe the cloning of full-length cDNA for sfrp1a, sfrp1b, sfrp2, sfrp3 and sfrp5 gene transcripts and we examine their expression at different embryonic stages. Only sfrp1a is expressed in the anterior neural plate including the ANB cells where and when tlc is expressed. Interestingly, compared to both tlc and sfrp1a, wnt genes are complementary expressed more posteriorly in the neural plate. Later, both sfrp1a and sfrp5 expression profiles are overlapping, in particular at pharyngula stage these genes are expressed in the ventral part of the forebrain, midbrain and hindbrain. sfrp1b, sfrp2 and sfrp3 are mainly expressed in mesodermal and endodermal embryonic tissues. Expression profiles of these different genes in zebrafish gave interesting clues on the possible function and evolution of sFRPs in zebrafish and other organisms.

Animals↗
PubMed1996

[Origin of the adenohypophysis and of the olfactory system in toads: demonstration by chimera method].

Localisation of the primordium of the olfactory system and its topographical relationships with the primordium of the hypothalamic-hypophyseal system were determined on the embryos of the toad Bufo japonicus by generating chimeric embryos. Different parts of the neural ridge and the neural plate were taken up from normal embryos and grafted on the same region of albino embryos of the same developmental stage. The melanin granules contained in the grafts permitted to trace the developmental fate. The anteriormost region of the neural ridge (ANR) was found to be the origin of all the parts of the adenohypophysis as well as some of the neurons in the preoptic region. The infundibulum differentiated from the central portion of the neural plate, just posterior to the adenohypophyseal primordium. The primordium of the olfactory system, including the olfactory sacs and the olfactory bulbs, was found to be situated on the neural ridge on both sides of the ANR. The present results showed that the central and peripheral parts of each of the two systems constitute a closely apposed cell population at the neurula stage. It seems that the periphero-central connection in these systems reflect a clonal origin of the presumptive cells. If the olfactory primordium was removed at the neurula stage, the olfactory sac regenerated from the adenohypophyseal primordium. In conclusion, these results demonstrate that the olfactory primordium is related not only topographically but also ontogenetically to the adenohypophyseal primordium.

Animals↗
PubMed2006

Cloning of vertebrate Protogenin (Prtg) and comparative expression analysis during axis elongation.

A murine cDNA encoding Protogenin, which belongs to the DCC/Neogenin family, was cloned in a screen performed to identify novel cDNAs regionally expressed in the neural plate. Isolation of the putative zebrafish orthologues allowed a comparative analysis of the expression patterns of Protogenin genes during embryogenesis in different vertebrate species. From mid-gastrulation to early somite stages, Protogenin expression is restricted to posterior neural plate and mesoderm, with an anterior limit at the level of the rhombencephalon in mouse, chicken, and zebrafish. During somitogenesis, the expression profiles in the three species share features in the neural tube but present also species-specific characteristics. The initiation of Protogenin expression just before somitogenesis and its maintenance in the neural tube and paraxial mesoderm during this process suggest a conserved role in axis elongation.

Amino Acid Sequence↗
PubMed1982

Intracellular sodium and the differentiation of amphibian embryonic neurones.

1. Experiments have been done to examine the mechanism of the inhibition of neural differentiation produced by inhibiting the sodium pump with cardiac glycosides during the mid-neural fold stages of development of the amphibian embryo. Neural differentiation was assessed quantitatively by counting the number of neurones that undergo primary differentiation in tissue culture, as a proportion of the total number of differentiated cells.2. Inhibition of the sodium pump by lowering the extracellular potassium concentration ([K(o)]) to 0 during the mid-neural fold stages inhibited neural differentiation.3. Raising the extracellular calcium concentration to 10 mM during treatment with strophanthidin protected differentiating neurones from the effects of the sodium pump inhibitor. Lowering [Ca](o) to 0.05 mM potentiated the effect of low doses of glycoside.4. In the presence of high extracellular calcium and 5 x 10(-6) M-strophanthidin the membrane potential of neural plate cells remained close to the levels recorded at the beginning of neurulation; the normal increase in resting potential was not restored.5. Addition of 10 mM-Sr(2+) to the bathing medium also protected nerve cells against the inhibition produced by strophanthidin; Sr(2+) was less effective than Ca(2+).6. Addition of either 10 mM-Mg(2+) or Mn(2+) had no effect on the inhibition of differentiation produced by strophanthidin.7. Addition of Mn(2+) along with high Ca(2+) prevented calcium from exerting its protective effect.8. The eyes of embryos treated with high Ca(2+) together with strophanthidin during neurulation and then allowed to grow into tadpoles developed normally. When Mn(2+) was present together with Ca(2+) and strophanthidin the eyes were disrupted similarly to those of embryos treated with strophanthidin alone.9. Replacement of extracellular sodium with equimolar amounts of choline or lithium prevented the cardiac glycoside from inhibiting neural differentiaion.10. The protection afforded by lowering [Na](o) was abolished when [Ca](o) was simultaneously lowered to 0.05 mM.11. Tadpoles from embryos treated with low extracellular sodium together with strophanthidin during neurulation had normal eyes compared to those treated with strophanthidin alone.12. Measurement of the intracellular sodium concentration ([Na](i)) with sodium-sensitive micro-electrodes put [Na](i) at about 30 mM before the neural folds lift. As the sodium pump is activated (stages 14(1/2)-15)[Na](i) in the neural plate falls; by the end of the mid-neural fold stage it is less than 10 mM.13. Addition of 5 x 10(-6)M-strophanthidin to the bathing fluid before activation of the sodium pump prevented the fall in [Na](i); in embryos where [Na](i) had begun to drop strophanthidin produced a rise to about 30 mM.14. When 10 mM-calcium was present along with strophanthidin [Na](i) fell to about 17 mM during neurulation, despite inhibition of the sodium pump.15. It is concluded that it is unlikely that either abolition of the normal increase in resting potential or a fall in gap junction permeability is responsible for the reduction in neural differentiation produced by blocking the sodium pump during neurulation.16. The results are consistent with the view that strophanthidin achieves its effect by preventing the fall in [Na](i) that occurs during normal neurulation because of activation of the sodium pump. They are discussed in the light of this suggestion.

Ambystoma mexicanum↗
PubMed2007

Convergent extension, planar-cell-polarity signalling and initiation of mouse neural tube closure.

Planar-cell-polarity (PCP) signalling is necessary for initiation of neural tube closure in higher vertebrates. In mice with PCP gene mutations, a broad embryonic midline prevents the onset of neurulation through wide spacing of the neural folds. In order to evaluate the role of convergent extension in this defect, we vitally labelled the midline of loop-tail (Lp) embryos mutant for the PCP gene Vangl2. Injection of DiI into the node, and electroporation of a GFP expression vector into the midline neural plate, revealed defective convergent extension in both axial mesoderm and neuroepithelium, before the onset of neurulation. Chimeras containing both wild-type and Lp-mutant cells exhibited mainly wild-type cells in the midline neural plate and notochordal plate, consistent with a cell-autonomous disturbance of convergent extension. Inhibitor studies in whole-embryo culture demonstrated a requirement for signalling via RhoA-Rho kinase, but not jun N-terminal kinase, in convergent extension and the onset of neural tube closure. These findings identify a cell-autonomous defect of convergent extension, requiring PCP signalling via RhoA-Rho kinase, during the development of severe neural tube defects in the mouse.

Animals↗
PubMed1991

Homeobox genes and models for patterning the hindbrain and branchial arches.

Antennapedia class homeobox genes, which in insects are involved in regional specification of the segmented central regions of the body, have been implicated in a similar role in the vertebrate hindbrain. The development of the hindbrain involves the establishment of compartments which are subsequently made distinct from each other by Hox gene expression, implying that the lineage of neural cells may be an important factor in their development. The hindbrain produces the neural crest that gives rise to the cartilages of the branchial skeleton. Lineage also seems to be important in the neural crest, as experiments have shown that the crest will form cartilages appropriate to its level of origin when grafted to a heterotopic location. We show how the Hox genes could also be involved in patterning the mesenchymal structures of the branchial skeleton. Recently it has been proposed that the rhombomere-restricted expression pattern of Hox 2 genes is the result of a tight spatially localised induction from underlying head mesoderm, in which a prepattern of Hox expression is visible. We find no evidence for this model, our data being consistent with the idea that the spatially localised expression pattern is a result of segmentation processes whose final stages are intrinsic to the neural plate. We suggest the following model for patterning in the branchial region. At first a segment-restricted code of Hox gene expression becomes established in the neuro-epithelium and adjacent presumptive neural crest. This expression is then maintained in the neural crest during migration, resulting in a Hox code in the cranial ganglia and branchial mesenchyme that reflects the crest's rhombomere of origin. The final stage is the establishment of Hox 2 expression in the surface ectoderm which is brought into contact with neural crest-derived branchial mesenchyme. The Hox code of the branchial ectoderm is established later in development than that of the neural plate and crest, and involves the same combination of genes as the underlying crest. Experimental observations suggest the idea of an instructive interaction between branchial crest and its overlying ectoderm, which would be consistent with our observations. The distribution of clusters of Antennapedia class genes within the animal kingdom suggests that the primitive chordates ancestral to vertebrates had at least one Hox cluster. The origin of the vertebrates is thought to have been intimately linked to the appearance of the neural crest, initially in the branchial region.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2004

Pbx genes are required in Xenopus lens development.

Development of the vertebrate eye is dependent on multiple tissue interactions and distinct sets of transcription factors and signalling molecules. The latter are thought to be FGF8 and BMP4, proteins secreted from the neural plate to induce lens formation in the overlying ectoderm. Here we show that the Pbx transcription factor plays a crucial role in this process, as it is required for FGF8 expression in the neural plate and is thus part of the complex hierarchy of genes involved in lens induction.

Animals↗
PubMed2000

Regulation and function of Dlx3 in vertebrate development.

Dlx3 is a homeodomain transcription factor in vertebrates, related to Distal-less in Drosophila, that is expressed in differentiating epidermal cells, in neural crest, hair follicles, dental epithelium and mesenchyme, the otic and olfactory placodes, limb bud, placenta, and in the cement gland, which is located in the extreme anterior neural plate in Xenopus embryos. This factor behaves as a transcriptional activator, and positively regulates gene expression in the skin, and negatively regulates central nervous system markers in Xenopus epidermis and anterior neural plate. A mutation in the DLX3 gene is associated with a hereditary syndrome in humans, and loss of Dlx3 function is a developmental lethal in gene-targeted mice, where it is essential for proper modeling of the labyrinthine layer of the placenta. In this review, we discuss the evolution, expression, regulation, and function of Dlx3 in mouse, amphibians, and zebrafish. Published 2000 Wiley-Liss, Inc.

Animals↗
PubMed2005

Patterning of proneuronal and inter-proneuronal domains by hairy- and enhancer of split-related genes in zebrafish neuroectoderm.

In teleosts and amphibians, the proneuronal domains, which give rise to primary-motor, primary-inter and Rohon-Beard (RB) neurons, are established at the beginning of neurogenesis as three longitudinal stripes along the anteroposterior axis in the dorsal ectoderm. The proneuronal domains are prefigured by the expression of basic helix-loop-helix (bHLH) proneural genes, and separated by domains (inter-proneuronal domains) that do not express the proneural genes. Little is known about how the formation of these domains is spatially regulated. We have found that the zebrafish hairy- and enhancer of split-related (Her) genes her3 and her9 are expressed in the inter-proneuronal domains, and are required for their formation. her3 and her9 expression was not regulated by Notch signaling, but rather controlled by positional cues, in which Bmp signaling is involved. Inhibition of Her3 or Her9 by antisense morpholino oligonucleotides led to ectopic expression of the proneural genes in part of the inter-proneuronal domains. Combined inhibition of Her3 and Her9 induced ubiquitous expression of proneural and neuronal genes in the neural plate, and abolished the formation of the inter-proneuronal domains. Furthermore, inhibition of Her3/Her9 and Notch signaling led to ubiquitous and homogeneous expression of proneural and neuronal genes in the neural plate, revealing that Her3/Her9 and Notch signaling have distinct roles in neurogenesis. These data indicate that her3 and her9 function as prepattern genes that link the positional dorsoventral polarity information in the posterior neuroectoderm to the spatial regulation of neurogenesis.

Animals↗
PubMed1992

Retinoic acid-induced neural tube defects with multiple canals in the chick: immunohistochemistry with monoclonal antibodies.

When retinoic acid was injected into chicken yolks before incubation, various types of neural tube defect (NTD) were induced in 38-46% of the embryos after 48-96 h of incubation. The cranial NTD consisted of a delay in closing of the neural plate in 48-h embryos and some remained as disorganized, hyperplastic masses in older embryos. In spinal NTD of 48-h embryos the posterior neuropore remained widely open. In older embryos with a closed posterior neuropore, the neural tube appeared dissociated or disorganized locally at the trunk level. The tissue consisted of a dorsally-situated, neural-plate-like structure and a ventrally-located cell mass containing multiple canals. Although the location was different, this arrangement was similar to the overlap zone which appears between primary and secondary neurulation in normal development. Immunohistochemistry was performed using monoclonal antibodies which selectively stained various components of chick tissue. Considering the similarity in neural tube formation between chick and human, this experimental NTD may provide clues to understanding the etiology of human myelomeningocele.

Animals↗
PubMed2003

A disrupted balance between Bmp/Wnt and Fgf signaling underlies the ventralization of the Gli3 mutant telencephalon.

Regionalization of the neural plate and the early neural tube is controlled by several signaling centers that direct the generation of molecularly distinct domains. In the developing telencephalon, the anterior neural ridge (ANR) and the roof and floor plate act as such organizing centers via the production of Fgfs, Bmps/Wnts, and Shh, respectively. It remains largely unknown, however, how the combination of these different signals is used to coordinate the generation of different telencephalic territories. In the present study, we report on telencephalic development in Pdn mutant mice, which carry an integration of a retrotransposon in the Gli3 locus. Homozygous mutant animals are characterized by a partial dorsal-to-ventral transformation of the telencephalon and by an increased size of the septum. On a molecular level, these alterations correlate with a reduction and/or loss of Bmp/Wnt expression and a concomitant expansion of Fgf8 transcription. Finally, we provide evidence that the ectopic activation of Fgf signaling in the dorsal telencephalon provides an explanation for the ventralization of the Gli3 mutant telencephalon as application of Fgf8-soaked beads to dorsal telencephalic explants led to the specific induction and repression of ventral marker and dorsal marker genes, respectively.

Animals↗
PubMed1998

Sequential roles for Otx2 in visceral endoderm and neuroectoderm for forebrain and midbrain induction and specification.

The homeobox gene Otx2 is a mouse cognate of the Drosophila orthodenticle gene, which is required for development of the brain, rostral to rhombomere three. We have investigated the mechanisms involved in this neural function and specifically the requirement for Otx2 in the visceral endoderm and the neuroectoderm using chimeric analysis in mice and explant recombination assay. Analyses of chimeric embryos composed of more than 90% of Otx2-/- ES cells identified an essential function for Otx2 in the visceral endoderm for induction of the forebrain and midbrain. The chimeric studies also demonstrated that an anterior neural plate can form without expressing Otx2. However, in the absence of Otx2, expression of important regulatory genes, such as Hesx1/Rpx, Six3, Pax2, Wnt1 and En, fail to be initiated or maintained in the neural plate. Using explant-recombination assay, we could further demonstrate that Otx2 is required in the neuroectodem for expression of En. Altogether, these results demonstrate that Otx2 is first required in the visceral endoderm for the induction, and subsequently in the neuroectoderm for the specification of forebrain and midbrain territories.

Animals↗
PubMed2001

A morphogen gradient of Wnt/beta-catenin signalling regulates anteroposterior neural patterning in Xenopus.

Anteroposterior (AP) patterning of the vertebrate neural plate is initiated during gastrulation and is regulated by Spemann's organizer and its derivatives. The prevailing model for AP patterning predicts a caudally increasing gradient of a 'transformer' which posteriorizes anteriorly specified neural cells. However, the molecular identity of the transforming gradient has remained elusive. We show that in Xenopus embryos (1) dose-dependent Wnt signalling is both necessary and sufficient for AP patterning of the neuraxis, (2) Wnt/beta-catenin signalling occurs in a direct and long-range fashion within the ectoderm, and (3) that there is an endogenous AP gradient of Wnt/beta-catenin signalling in the presumptive neural plate of the Xenopus gastrula. Our results indicate that an activity gradient of Wnt/beta-catenin signalling acts as transforming morphogen to pattern the Xenopus central nervous system.

Animals↗
PubMed1998

Glycoconjugate expression during early mouse oculogenesis.

The carbohydrate side-chain of glycoconjugates can show a developmentally regulated expression pattern. In order to analyse these changes during the development of the eye, 13 lectins were used to reveal glycoconjugates histochemically in 8.5- to 14-day-old mouse embryos. During this period, eyes develop from the most immature vesiculation of the neural plate neuroepithelium into a primitive stage with all structures present, such as pigment epithelium, not yet differentiated neuroretina and lens. A striking diversity of carbohydrate side-chain expression was observed in the preocular somatoectoderm and neural plate of 8.5-day-old embryos, as indicated by the binding of nine different lectins. Binding sites at the apical poles of neuroepithelium of five of these lectins (PNA, LCA, SBA, LPA and GSA-II) disappeared completely during further development. The binding sites of four other lectins, WGA, MPA, Con A and BPA, remained expressed during the course of development, being indicative for the carbohydrate side-chains beta-GlcNAc(1-4)Gluc, alpha-Gal(1-3)GalNAc, alpha-D-Man/alpha-D-Gluc and alpha-GalNAc. In contrast, binding sites for GSA-I, RCA-I (alpha-D-Gal), UEA-I (alpha-L-Fuc) and DBA (alpha-GalNAc(1-3)GalNAc) were not present at any developmental stage. The time point of gross changes of lectin binding sites correlates well with the period of neural tube formation. During later development from neuroectoderm to the ocular pigment epithelium, a sharp reduction in all lectin binding sites at the apical cell poles, except for WGA and MPA, was observed. WGA binding sites were present until embryonic day 10, while those for MPA were present until day 9. At the basal cell poles of the pigment epithelium, all lectin binding sites except for WGA were lost after embryonic day 11.5. These results indicate that there are sophisticated kinetics of glycoconjugate expression during the course of early embryonic development of ectoderm into its descendent tissues.

Animals↗
PubMed2005

A balance of FGF, BMP and WNT signalling positions the future placode territory in the head.

The sensory nervous system in the vertebrate head arises from two different cell populations: neural crest and placodal cells. By contrast, in the trunk it originates from neural crest only. How do placode precursors become restricted exclusively to the head and how do multipotent ectodermal cells make the decision to become placodes or neural crest? At neural plate stages, future placode cells are confined to a narrow band in the head ectoderm, the pre-placodal region (PPR). Here, we identify the head mesoderm as the source of PPR inducing signals, reinforced by factors from the neural plate. We show that several independent signals are needed: attenuation of BMP and WNT is required for PPR formation. Together with activation of the FGF pathway, BMP and WNT antagonists can induce the PPR in naïve ectoderm. We also show that WNT signalling plays a crucial role in restricting placode formation to the head. Finally, we demonstrate that the decision of multipotent cells to become placode or neural crest precursors is mediated by WNT proteins: activation of the WNT pathway promotes the generation of neural crest at the expense of placodes. This mechanism explains how the placode territory becomes confined to the head, and how neural crest and placode fates diversify.

Animals↗
PubMed1999

Development of noradrenergic neurons in the zebrafish hindbrain requires BMP, FGF8, and the homeodomain protein soulless/Phox2a.

We report that the zebrafish mutation soulless, in which the development of locus coeruleus (LC) noradrenergic (NA) neurons failed to occur, disrupts the homeodomain protein Phox2a. Phox2a is not only necessary but also sufficient to induce Phox2b+ dopamine-beta-hydroxylase+ and tyrosine hydroxylase+ NA neurons in ectopic locations. Phox2a is first detected in LC progenitors in the dorsal anterior hindbrain, and its expression there is dependent on FGF8 from the mid/hindbrain boundary and on optimal concentrations of BMP signal from the epidermal ectoderm/future dorsal neural plate junction. These findings suggest that Phox2a coordinates the specification of LC in part through the induction of Phox2b and in response to cooperating signals that operate along the mediolateral and anteroposterior axes of the neural plate.

Amino Acid Sequence↗
PubMed1995

Tail bud determination in the vertebrate embryo.

BACKGROUND: Although as humans we lose our tails in the second month of embryonic development, a persistent tail is a prominent structural feature of most adult vertebrates. Indeed, the post-anal tail is part of the definition of a chordate. The internal organization of the developing tail--with neural tube, notochord and paired somites--is the same as that of the main body axis, so it can be expected that the mechanism of tail formation has a close relationship to that of the vertebrate body plan as a whole. Despite this, almost nothing is known about how tails arise. RESULTS: We present evidence to show that the tail bud of Xenopus laevis arises as the result of interactions between distinct zones of tissue at the posterior of the embryo at the neurula stage. These tissue interactions were demonstrated by manipulations of exogastrulae, which normally form no tail, and by transplantation experiments performed on the neural plate of stage 13 neurulae, whereby embryos with supernumary tails were produced. CONCLUSIONS: We propose a new model of tail bud determination, termed the NMC model, to explain the results we have obtained. In this model, the tail bud is initiated by an interaction between two territories in the neural plate and a posterior mesodermal territory.

Animals↗