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PubMed1999

Establishment and maintenance of the border of the neural plate in the chick: involvement of FGF and BMP activity.

We have investigated the cell interactions and signalling molecules involved in setting up and maintaining the border between the neural plate and the adjacent non-neural ectoderm in the chick embryo at primitive streak stages. msx-1, a target of BMP signalling, is expressed in this border at a very early stage. It is induced by FGF and by signals from the organizer, Hensen's node. The node also induces a ring of BMP-4, some distance away. By the early neurula stage, the edge of the neural plate is the only major site of BMP-4 and msx-1 expression, and is also the only site that responds to BMP inhibition or overexpression. At this time, the neural plate appears to have a low level of BMP antagonist activity. Using in vivo grafts and in vitro assays, we show that the position of the border is further maintained by interactions between non-neural and neural ectoderm. We conclude that the border develops by integration of signals from the organizer, the developing neural plate, the paraxial mesoderm and the non-neural epiblast, involving FGFs, BMPs and their inhibitors. We suggest that BMPs act in an autocrine way to maintain the border state.

Animals↗
PubMed2002

Fate map of the chicken neural plate at stage 4.

A detailed fate map was obtained for the early chick neural plate (stages 3d/4). Numerous overlapping plug grafts were performed upon New-cultured chick embryos, using fixable carboxyfluorescein diacetate succinimidyl ester to label donor chick tissue. The specimens were harvested 24 hours after grafting and reached in most cases stages 9-11 (early neural tube). The label was detected immunocytochemically in wholemounts, and cross-sections were later obtained. The positions of the graft-derived cells were classified first into sets of purely neural, purely non-neural and mixed grafts. Comparisons between these sets established the neural plate boundary at stages 3d/4. Further analysis categorized graft contributions to anteroposterior and dorsoventral subdivisions of the early neural tube, including data on the floor plate and the eye field. The rostral boundary of the neural plate was contained within the earliest expression domain of the Ganf gene, and the overall shape of the neural plate was contrasted and discussed with regard to the expression patterns of the genes Plato, Sox2, Otx2 and Dlx5 (and others reported in the literature) at stages 3d/4.

Animals↗
PubMed2005

Convergence of Wnt and FGF signals in the genesis of posterior neural plate through activation of the Sox2 enhancer N-1.

The expression of the transcription factor gene Sox2 precisely marks the neural plate in various vertebrate species. We previously showed that the Sox2 expression prevailing in the neural plate of chicken embryos is actually regulated by the coordination of five phylogenetically conserved enhancers having discrete regional coverage, among which the 420-bp long enhancer N-1, active in the node-proximal region, is probably involved directly in the genesis of the posterior neural plate. We investigated the signaling systems regulating this enhancer, first identifying the 56-bp N-1 core enhancer (N-1c), which in a trimeric form recapitulates the activity of the enhancer N-1. Mutational analysis identified five blocks, A to E, that regulate the enhancer N-1c. Functional analysis of these blocks indicated that Wnt and FGF signals synergistically activate the enhancer through Blocks A-B, bound by Lef1, and Block D, respectively. Fgf8b and Wnt8c expressed in the organizer-primitive streak region account for the activity in the embryo. Block E is essential for the repression of the enhancer N-1c activity in the mesendodermal precursors. The enhancer N-1c is not affected by BMP signals. Thus, Wnt and FGF signals converge to activate Sox2 expression through the enhancer N-1c, revealing the direct involvement of the Wnt signal in the initiation of neural plate development.

Animals↗
PubMed2000

Fate mapping of the mouse prosencephalic neural plate.

Little is known about the behavior of cells within the anterior neural plate or tube in developing mammalian embryos in utero due to technical limitations. Here we labeled neuroepithelial cells with vital dye and traced their siblings for 1 or 2 days using the whole-embryo culture system. The results demonstrated that rostral cell movement from the midbrain to the forebrain in the mouse neural plate was restricted at the boundary by the five-somite stage. Coincident with restriction of cell intermingling, expression of a transcription factor, Pax6, and a cell adhesion molecule, cadherin-6, commmenced to demarcate the forebrain compartment. Within this compartment, we also mapped several prospective regions of the telencephalon and diencephalon to the eyes. The fate map of the mouse prosencephalic neural plate was very similar to those of other vertebrates, providing evidence that mammalian-specific brain structures, represented in the cerebral neocortex, could evenly develop along the conserved framework of neuromeres.

Amino Acid Sequence↗
PubMed2000

The olfactory placodes of the zebrafish form by convergence of cellular fields at the edge of the neural plate.

The primary olfactory sensory system is part of the PNS that develops from ectodermal placodes. Several cell types, including sensory neurons and support cells, differentiate within the olfactory placode to form the mature olfactory organ. The olfactory placodes are thought to arise from lateral regions of the anterior neural plate, which separate from the plate through differential cell movements. We determined the origins of the olfactory placodes in zebrafish by labeling cells along the anterior-lateral edge of the neural plate at times preceding the formation of the olfactory placodes and examining the later fates of the labeled cells. Surprisingly, we found that the olfactory placode arises from a field of cells, not from a discrete region of the anterior neural plate. This field extends posteriorly to the anterior limits of cranial neural crest and is bordered medially by telencephalic precursors. Cells giving rise to progeny in both the olfactory organ and telencephalon express the distal-less 3 gene. Furthermore, we found no localized pockets of cell division in the anterior-lateral neural plate cells preceding the appearance of the olfactory placode. We suggest that the olfactory placodes arise by anterior convergence of a field of lateral neural plate cells, rather than by localized separation and proliferation of a discrete group of cells.

Animals↗
PubMed1999

Expression of Pax-3 in the lateral neural plate is dependent on a Wnt-mediated signal from posterior nonaxial mesoderm.

During early patterning of the vertebrate neuraxis, the expression of the paired-domain transcription factor Pax-3 is induced in the lateral portions of the posterior neural plate via posteriorizing signals emanating from the late organizer and posterior nonaxial mesoderm. Using a dominant-negative approach, we show in explant assays that Pax-3 inductive activities from the organizer do not depend on FGF, retinoic acid, or XWnt-8, either alone or in combination, suggesting that the organizer may produce an unknown posteriorizing factor. However, Pax-3 inductive signals from posterior nonaxial mesoderm are Wnt-dependent. We show that Pax-3 expression in the lateral neural plate expands in XWnt-8-injected embryos and is blocked by dominant-negative XWnt-8. Similarly, we show that the homeodomain transcription factor Msx-1, which like Pax-3 is an early marker of the lateral neural plate, is induced by posterior nonaxial mesoderm and blocked by dominant-negative XWnt-8. Finally, we show that Rohon-Beard primary neurons, a cell type that develops within the lateral neural plate, are also blocked in vivo by dominant-negative Xwnt-8. Together these data support a model in which patterning of the lateral neural plate by Wnt-mediated signals is an early event that establishes a posteriolateral domain, marked by Pax-3 and Msx-1 expression, from which Rohon-Beard cells and neural crest will subsequently arise.

Animals↗
PubMed1997

Expression of Pax-3 is initiated in the early neural plate by posteriorizing signals produced by the organizer and by posterior non-axial mesoderm.

Pax-3 is a paired-type homeobox gene that is specifically expressed in the dorsal and posterior neural tube. We have investigated inductive interactions that initiate Pax-3 transcript expression in the early neural plate. We present several lines of evidence that support a model where Pax-3 expression is initiated by signals that posteriorize the neuraxis, and then secondarily restricted dorsally in response to dorsal-ventral patterning signals. First, in chick and Xenopus gastrulae the onset of Pax-3 expression occurs in regions fated to become posterior CNS. Second, Hensen's node and posterior non-axial mesoderm which underlies the neural plate induce Pax-3 expression when combined with presumptive anterior neural plate explants. In contrast, presumptive anterior neural plate explants are not competent to express Pax-3 in response to dorsalizing signals from epidermal-ectoderm. Third, in a heterospecies explant recombinant assay with Xenopus animal caps (ectoderm) as a responding tissue, late, but not early, Hensen's node induces Pax-3 expression. Chick posterior non-axial mesoderm also induces Pax-3, provided that the animal caps are neuralized by treatment with noggin. Finally we show that the putative posteriorizing factors, retinoic acid and bFGF, induce Pax-3 in neuralized animal caps. However, blocking experiments with a dominant-inhibitory FGF receptor and a dominant-inhibitory retinoic acid receptor suggest that Pax-3 inductive activities arising from Hensen's node and posterior non-axial mesoderm do not strictly depend on FGF or retinoic acid.

Animals↗
PubMed2001

The circadian gene Clock is restricted to the anterior neural plate early in development and is regulated by the neural inducer noggin and the transcription factor Otx2.

The circadian cycle is a simple, universal molecular mechanism for imposing cyclical control on cellular processes. Here we have examined the regulation of one of the key circadian genes, Clock, in early Xenopus development. We find that the expression of Clock is dependent on developmental stage, not on time per se, and is mostly restricted to the anterior neural plate. It's expression can be induced by the secreted polypeptide noggin, and subsequently upregulated by Otx2, a transcription factor required for the determination of anterior fate.

Animals↗
PubMed1988

Development of the central nervous system of the larva of the ascidian, Ciona intestinalis L. I. The early lineages of the neural plate.

The early lineages of the larval central nervous system (CNS) of the ascidian, Ciona intestinalis, have been traced using scanning electron microscopy (SEM) of embryos fixed at 12-min intervals. The CNS precursors lie superficially, exposed for a long portion (9.3 hr of 42%) of embryonic development, in the neural plate. In the 64-cell stage embryo the neural plate contains 10 cells; in all but the first vegetal division these divide with transverse cleavage planes. Synchrony is progressively lessened, but temporal sequence is always exact. Successive divisions occur initially at 30-min intervals. Our analysis confirms existing lineage descriptions for the neural plate up to the end of gastrulation and advances the lineage record through the crucial and temporally complex ninth cleavage, during which cells divide by the following rules: medial cells in each row divide first; the anterior row of vegetal daughter cells divides before their posterior siblings; the posterior row of animal daughter cells divide before their anterior siblings. All cells attain their 10th generation, but four cannot be followed by SEM. In preparation for neurulation the neural plate then comprises 76 cells, forming up to four rows each of eight vegetal hemisphere cells located on the dorsal surface of the embryo, anterior to the blastopore, and eight rows each of six animal hemisphere cells, located anterior to the rows of eight. The temporal and spatial patterns of early cleavage stages have been confirmed in vivo by observations using Nomarski optics.

Animals↗
PubMed1986

The histogenetic potential of neural plate cells of early-somite-stage mouse embryos.

The mesencephalic neural plate of early-somite-stage mouse embryos differentiated underneath the renal capsule to form mostly neural tissues together with other tissues some of which were probably of neural crest cell origin. The capacity to form non-neural tissues such as skeletal tissues and melanocytes was lost at about the 5-somite stage. The lateral areas of the plate tended to form non-neural tissues more than the medial areas. The cephalic neural plate of presomite head-fold-stage embryos differentiated extensively to form both ectodermal and mesodermal tissues. However, upon completion of neurulation, the mesencephalic neuroepithelium of forelimb-bud-stage embryos gave rise to neural tissues only. Therefore there is a progressive restriction in the histogenetic capacity of the mesencephalic neural plate during neurulation and this could be attributed to the cellular commitment for neural differentiation and the loss of the neural crest cells.

Animals↗
PubMed1999

Ectodermal patterning in the avian embryo: epidermis versus neural plate.

Ectodermal patterning of the chick embryo begins in the uterus and continues during gastrulation, when cells with a neural fate become restricted to the neural plate around the primitive streak, and cells fated to become the epidermis to the periphery. The prospective epidermis at early stages is characterized by the expression of the homeobox gene DLX5, which remains an epidermal marker during gastrulation and neurulation. Later, some DLX5-expressing cells become internalized into the ventral forebrain and the neural crest at the hindbrain level. We studied the mechanism of ectodermal patterning by transplantation of Hensen's nodes and prechordal plates. The DLX5 marker indicates that not only a neural plate, but also a surrounding epidermis is induced in such operations. Similar effects can be obtained with neural plate grafts. These experiments demonstrate that the induction of a DLX5-positive epidermis is triggered by the midline, and the effect is transferred via the neural plate to the periphery. By repeated extirpations of the endoderm we suppressed the formation of an endoderm/mesoderm layer under the epiblast. This led to the generation of epidermis, and to the inhibition of neuroepithelium in the naked ectoderm. This suggests a signal necessary for neural, but inhibitory for epidermal development, normally coming from the lower layers. Finally, we demonstrate that BMP4, as well as BMP2, is capable of inducing epidermal fate by distorting the epidermis-neural plate boundary. This, however, does not happen independently within the neural plate or outside the normal DLX5 domain. In the area opaca, the co-transplantation of a BMP4 bead with a node graft leads to the induction of DLX5, thus indicating the cooperation of two factors. We conclude that ectodermal patterning is achieved by signalling both from the midline and from the periphery, within the upper but also from the lower layers.

Animals↗
PubMed2005

Agreement and disagreement among fate maps of the chick neural plate.

Fate maps are essential to understand embryonic development; they provide a background for deducing maps of differential cellular specification in the context of other experimental data and molecular expression patterns. Due to its accessibility, the chick neural plate has been fate-mapped many times, albeit without complete agreement with respect to its shape, extent and fated subdivisions. In this review, we first comment about avian neural plate fate maps reported since the early period of experimental embryology, referring to the different methods followed. We next review a perfected fate-mapping methodology, which recently allowed us rather precise delimitation of the chick neural plate at stages 3d/4. This leads to a general discussion about the apparent border of the neural plate and the prospective main rostrocaudal and longitudinal divisions of the neural tube.

Animals↗
PubMed1993

Lineage analysis of early neural plate cells: cells with purely neuronal fate coexist with bipotential neuroglial progenitors.

To investigate the lineage relationships of neurons and astroglial cells early in central nervous system development, we have analyzed the progeny of neural plate cells in an amphibian embryo (Pleurodeles waltl). A fluorescent tracer, lysinated rhodamine-dextran, was iontophoretically injected into individual precursor cells in various areas of the early neural plate. The phenotypes of clonally related cells were identified in the hindbrain and spinal cord by morphological and immunohistochemical criteria 12 days later, at larval stages. We found that the large majority of clones (83%) contained both neurons and astroglial cells, whereas the remainder (17%) were homogeneous and were only composed of neurons. We never observed purely astroglial clones. These results clearly demonstrate the predominance of bipotential progenitors in the neural plate. Interestingly, the progenitors with a restricted neuronal fate were always located along the intermediate axes of the neural plate, while mixed progenitors were found in all areas examined. The analysis of migratory paths has shown that sister cells first migrated together along radial pathways without dispersion along the rostrocaudal axis. From larval stages, some neurons migrated away from the original clonal cohort along dorsoventral and ventrodorsal tangential routes, but only after they had reached the border between the intermediate and marginal zones.

Animals↗
PubMed1999

Bending of the neural plate during mouse spinal neurulation is independent of actin microfilaments.

To examine the role of actin microfilaments in mouse spinal neurulation, we stained cryosections of E8.5-10.5 CBA/Ca embryos with FITC-phalloidin. Microfilaments are present in the apical region of all cells throughout the neuroepithelium, irrespective of whether they are involved in bending of the neural plate. Disruption of the microfilaments with cytochalasin D inhibited closure of the cranial neural folds in cultured embryos, even at the lowest concentrations tested, and prevented the initiation of spinal neurulation (Closure 1) at higher concentrations. In contrast, closure of the posterior neuropore was resistant to cytochalasin D at the highest concentrations tested. Phalloidin staining and transmission electron microscopy confirmed that cytochalasin D is effective in disassembling microfilaments in spinal neuroepithelial cells. We conclude that spinal neural tube closure does not require microfilament function, in contrast to cranial neurulation which is strongly microfilament-dependent. Histological examination of cytochalasin D-treated embryos revealed that bending at hinge points, both in the midline (MHP) and dorsolaterally (DLHPs), continues in the absence of microfilaments, whereas the rigidity of non-bending regions of the neural plate is lost. This suggests that spinal neurulation can continue in the presence of cytochalasin D largely as a result of intrinsic bending of the neural plate at hinge points. Cytochalasin D treatment is a useful tool for revealing the localisation of hinge points in the neural plate. Analysis of treated embryos demonstrates a transition, along the spinal axis, from closure solely involving midline bending, at high levels of the spinal axis, to closure solely involving dorsolateral bending, low in the spinal region. These findings support the idea of mechanistic heterogeneity in mouse neurulation, along the body axis, and demonstrate that contraction of actin microfilaments is not obligatory for epithelial bending during embryonic morphogenesis. Dev Dyn 1999;215:273-283.

Actin Cytoskeleton↗
PubMed1995

A homeobox gene involved in node, notochord and neural plate formation of chick embryos.

We have isolated a chicken cDNA clone, Cnot, resembling in sequence and expression pattern the Xenopus homeobox gene Xnot. The major, early transcription domains of Cnot are the node, the notochord and prenodal and postnodal neural plate caudal from the prospective hindbrain level. All these cell populations appear to be descendants of the Cnot-expressing cells of the node, suggesting a cell lineage relationship. After the onset of somitogenesis, a second, independent expression domain appears in the neural folds at the prospective mid- and forebrain levels, and further transcripts are found in the epiphysis, the ventral diencephalon, the preoral gut and the limb buds. Transplantation of nodes from extended streak embryos leads to the formation of ectopic notochords, which express Cnot in the typical, cranially decreasing gradient. Transplantation of young nodes to young hosts has previously been described to induce secondary embryos. We observed that secondary chick embryos express Cnot in node derived, notochord-like structures and in the anterior neural plate, similar to the domains seen in primary embryos. However, expression was absent from the posterior neural plate, which in the induction experiments is excluded from the node lineage. This finding corroborates our initial conclusion about a cell lineage relationship between node, notochord, and neural plate defined by Cnot expression. The midline mesoderm of vertebrate embryos consists of two tissues, the prechordal mesoderm and the notochord. The anterior notochord, the head process, may represent an intermediate form. The transition from prechordal to chordal mesoderm can be followed by the expression of the two marker homeobox genes goosecoid and Cnot, first in the primitive streak, and then in the head process. We suggest that expression of goosecoid or Cnot is involved in the specification of a prechordal or notochordal identity, respectively. A transition from goosecoid to Cnot expression may proceed, while cells are still in the epiblast, but not after becoming mesodermal. A molecular coding of axial positions in the midline mesoderm may occur by specific homeobox genes, similar to the situation in the neural tube and the somitic mesoderm.

Amino Acid Sequence↗
PubMed1995

Dorsal differentiation of neural plate cells induced by BMP-mediated signals from epidermal ectoderm.

The cellular interactions that control the differentiation of dorsal cell types from neural progenitors have been examined in neural plate explants. Certain genes that are expressed in the dorsal neural tube are initially expressed uniformly within the neural plate and appear to achieve their dorsal restriction through a Sonic hedgehog (SHH)-mediated repressive signal from the notochord. The acquisition of definitive dorsal cell fates, however, requires a contact-dependent signal from the epidermal ectoderm. BMP4 and BMP7 are expressed in the epidermal ectoderm, and both proteins mimic its inductive activity. BMP4 and a related gene, DSL1, are subsequently expressed by cells in the dorsal neural tube. The differentiation of dorsal cell types, therefore, appears to be initiated at the neural plate stage and to involve the opponent activities of a BMP-mediated dorsalizing signal from the epidermal ectoderm and a SHH-mediated ventralizing signal from the notochord.

Animals↗
PubMed1984

Quantitative analyses of changes in cell shapes during bending of the avian neural plate.

It is widely believed that changes in cell shapes play important roles in the bending or folding of epithelial sheets, but few studies have actually examined cell shapes in such systems. We have determined the percentages of four types of neuroepithelial cells (i.e., spindle, flask, inverted flask, and globular) present during bending of the avian neural plate. Serial transverse plastic sections through seven craniocaudal levels of the neuroepithelium were examined. Four distinct periods of bending were chosen based on the morphology of the neuroepithelium: period I, flat neural plate; period II, midline furrow without elevation of the neural folds; period III, midline furrow with elevation; and period IV, bilateral furrows with convergence of the neural folds. We compared statistically the percentages of different cell types in bending (furrowed) and nonbending regions of the neuroepithelium, as well as changes in cell shapes with time. Our results demonstrate that dramatic changes in cell shapes occur in the midline and bilateral furrows during bending of the neural plate, such that as many as 70% of the neuroepithelial cells in the midline and 55% in the bilateral furrows are wedge shaped by the end of bending. In contrast, less than 35% of the neuroepithelial cells are wedge shaped outside of the three morphological loci of bending. These results support the hypothesis that localized changes in cell morphologies have roles in bending and shaping of the neural plate, but exactly how cells change shapes and what precise roles such changes play in bending remain to be determined.

Animals↗
PubMed1993

Glucose causes lengthening of the microvilli of the neural plate of the rat embryo and produces a helical pattern on their surface.

Prominent microvilli have been observed on the surface of neural plates in the embryos of many species. Since glucose is the main source of energy for embryos before neural tube closure and the onset of vascular circulation, it was of interest to study the relationship between these microvilli and glucose utilization in the neural plate. By applying microdrops of amniotic fluid to chemstrips, which colorimetrically measure glucose by glucose oxidase reaction, we determined that day 10 rat amniotic fluid glucose level was 31.6 +/- 1.6 mg/dl. On day 10 and within about 20 min from removal of the decidual sites, no glucose was found in the amniotic fluid. By use of a scanning electron microscope, the microvilli of the day 10 neural plate were found to have a 10-fold increase in length during a 40-min exposure to Hanks' solution at 21-23 degrees C. Similarly exposed embryos in Hanks' without glucose did not have microvillus elongation. However, under whole embryo culture conditions at 38 degrees C no extension of the microvilli was found. In the closed neural tube of the day 10 embryo, the microvilli were stubby and did not elongate with glucose exposure. Similarly, day 11 and 14 embryos had short microvilli which did not elongate with direct exposure to glucose at 21-23 degrees C. The short microvilli on the surface of the closed neural tube on day 11, 14, and 16 were associated with low glucose concentrations in the neural tube fluids. By use of a field emission scanning electron microscope, the surfaces of the microvilli in the extended position were seen to be covered by a right-handed helical array of globular objects the size of large molecules. The findings support the hypothesis that microvillar length may modulate glucose uptake. Shortening is associated with low concentrations of glucose in closed neural tubes, and lengthening occurs at glucose exposures of 100 mg/dl.

Amniotic Fluid↗