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PubMed2001

The ectodermal placodes: a dysfunctional family.

The ectodermal placodes are focal thickenings of the cranial embryonic ectoderm that contribute extensively to the cranial sensory systems of the vertebrates. The ectodermal placodes have long been thought of as representing a coherent group, which share a developmental and evolutionary history. However, it is now becoming clear that there are substantial differences between the placodes with respect to their early development, their induction and their evolution. Indeed, it is now hard to consider the ectodermal placodes as a single entity. Rather, they fall into a number of distinct classes and it is within each of these that the members share a common development and evolution.

Animals↗
PubMed1987

Spec3: embryonic expression of a sea urchin gene whose product is involved in ectodermal ciliogenesis.

We have characterized the temporal and spatial expression of Spec3 mRNA in embryos of the sea urchin, Strongylocentrotus purpuratus. This mRNA, 2.0 kb in length, is present at low levels in unfertilized eggs but accumulates rapidly during cleavage, increasing 50-fold by hatching blastula stage. Message levels then decline abruptly, remain constant during mesenchyme blastula and gastrula stages, and increase again during prism and pluteus stages. This accumulation pattern is quite similar to that of the ectodermally expressed beta-tubulin mRNAs described recently by Harlow and Nemer (1987a). In situ hybridization shows that although Spec3 message accumulates in all blastomeres at early blastula stages, it later becomes restricted to ectoderm. By late blastula stage, hybridization is strongest in the animal hemisphere. At gastrula, signals are variable over ectoderm, and by pluteus, grains are concentrated in the ciliary band, though present in other ectodermal cells as well. Deciliation and regeneration of cilia in gastrula-stage embryos results in a four- to fivefold increase in Spec3 mRNA levels, implying that the Spec3 gene product is associated with ciliogenesis. Spec3 mRNA is encoded by a single gene in the haploid genome, and characterization of the gene shows that it contains three exons that encode an open reading frame for a hydrophobic protein of 21.6 kD. The reading frame reveals that the carboxy-terminal part of the protein contains two long hydrophobic stretches, 31 and 37 residues long, separated by short hydrophilic regions of six to eight residues. The presence of these two distinct hydrophobic stretches suggests that the Spec3 protein contains two alpha-helical domains that either span the lipid bilayer or are associated with some other hydrophobic environment.

Amino Acid Sequence↗
PubMed1989

Progressively restricted expression of a homeo box gene within the aboral ectoderm of developing sea urchin embryos.

A homeo box-containing gene, Hbox1 is expressed in an unusual and highly conserved spatial pattern in embryos of two different species of sea urchin, Tripneustes gratilla and Strongylocentrotus purpuratus. Hybridization in situ shows that this mRNA accumulates initially throughout the aboral ectoderm; however, between blastula and pluteus stages, the region containing Hbox1 mRNA retracts gradually until only a small area around the vertex is labeled in pluteus larvae. Aboral ectoderm appears cytologically uniform and also accumulates uniform levels of other tissue-specific mRNAs. Therefore, the Hbox1 pattern reveals a previously unsuspected heterogeneity of aboral ectoderm cells and a polarity within this tissue. In S. purpuratus, the Hbox1 gene product probably is not involved in initial specification of cell fate, as this message does not achieve a significant fraction of its peak abundance until almost hatching blastula stage, well after the time aboral ectoderm cells have initiated a tissue-specific program of gene expression. RNA blot and RNase protection analyses revealed low levels of Hbox1 mRNA in all adult tissues examined. However, this message was not detectable in mature eggs, suggesting that the Hbox1 gene does not have a maternal function. In addition to highly conserved spatial and temporal patterns of expression, the homeo box genes of these two urchin species also are conserved highly in sequences outside the homeo domain, despite the divergence of these two species (30-45 my). Two notable features of the protein shared with several vertebrate homeo proteins are a short conserved sequence encoded by an exon upstream of that encoding the homeo domain and a large region of high serine and proline content.

Amino Acid Sequence↗
PubMed1995

Disruption of BMP signals in embryonic Xenopus ectoderm leads to direct neural induction.

Bone morphogenetic proteins (BMPs), which have been implicated in the patterning of mesoderm, are members of the transforming growth factor-beta (TGF-beta) superfamily. We have investigated the roles of Xenopus BMP-7 (XBMP-7) and BMP-4 (XBMP-4), and activin (another TGF-beta-related molecule) in early development by generating dominant-negative versions of these growth factors. Mutations were generated by altering the cleavage sites that are required for maturation of the active dimeric forms of XBMP-7, XBMP-4, and activin. These mutant constructs, designated Cm-XBMP-7, Cm-XBMP-4, and Cm-activin, result in polypeptides that allow for dimerization of the subunits, but are incapable of maturation. Expression of Cm-XBMP-7 and Cm-XBMP-4, but not Cm-activin, in the ventral marginal zone of the Xenopus embryo results in the development of a secondary axis, similar to that seen by ectopic expression of the truncated BMP receptor. These results suggest that the cleavage mutants interfere with BMP signaling during mesodermal patterning. We also found that expression of Cm-XBMP-7 or Cm-XBMP-4 in animal cap ectoderm directly induces neuroectoderm. The neural induction was specific for Cm-XBMP-7 and Cm-XBMP-4 because ectopic expression of Cm-activin or Vg-1 did not mimic the same phenotype. Molecular study of neural patterning by Cm-XBMP-7 and Cm-XBMP-4 revealed that only anterior neuroectodermal markers are expressed in response to these Cm-XBMPs. These results suggest that the BMPs are involved in the specification of ectoderm in Xenopus development, and that neural induction requires the removal of BMP signals in the ectoderm. We propose that neural induction occurs by a default mechanism, whereby the inhibition of BMP signaling is required for the conversion of ectoderm to neuroectoderm in the developing Xenopus embryo.

Activins↗
PubMed2004

Ectodermal dysplasia showing clinical overlap between AEC, Rapp-Hodgkin and CHAND syndromes.

The ectodermal dysplasias represent a complex collection of congenital abnormalities of skin, hair, teeth, nail, and sweat gland development, many of which have overlapping clinical features. In this report, we describe a 7-year-old girl, born to clinically normal parents, with ankyloblepharon, cleft lip/palate and hair abnormalities, features resembling the autosomal dominant disorder, ankyloblepharon-ectodermal dysplasia-clefting (AEC) syndrome, which results from mutations in the sterile-alpha motif domain of the gene encoding the transcription factor, p63. However, direct sequencing of the p63 gene in this individual did not reveal any pathogenic sequence variants. Moreover, two of her paternal cousins were discovered to have similar congenital ectodermal anomalies, raising the alternative possibility of an autosomal recessive pattern of inheritance. Furthermore, all affected individuals lacked a history of erosive scalp dermatitis that is usually characteristic of AEC syndrome. Instead, the scalp hair was coarse and wiry. In addition, another atypical feature, hypohidrosis, was present. Collectively, the clinical features also resembled Rapp-Hodgkin syndrome, Bowen-Armstrong syndrome and CHAND syndrome, but did not appear to fit neatly with any one particular disorder. This case highlights the difficulties in trying to classify the ectodermal dysplasia syndromes on clinical features alone.

Child↗
PubMed2004

ADULT ectodermal dysplasia syndrome resulting from the missense mutation R298Q in the p63 gene.

Several ectodermal dysplasia syndromes have been shown to result from mutations in the gene that encodes the transcription factor p63. We describe an 11-year-old boy, with clinically normal parents, who had a developmental disorder that resembled EEC (ectrodactyly ectodermal dysplasia-clefting) syndrome (OMIM 604292). He had ectrodactyly and missing middle fingers bilaterally, onychodysplasia, hypodontia with missing teeth, hypohidrosis and lacrimal duct obstruction. DNA sequencing disclosed a heterozygous G-->A substitution at nucleotide 893, that converts an arginine residue (CGA) to glutamine (CAA), the mutation being designated R298Q. This mutation occurs within the DNA-binding domain of p63, and is close to many of the published EEC syndrome mutations. However, R298Q has been described once previously in a large German pedigree, not with EEC syndrome, but another ectodermal dysplasia disorder, ADULT (acro-dermato-ungual-lacrimal-tooth) syndrome (OMIM 103285). Further clinical assessment in our patient revealed that, apart from not having cleft lip and/or palate, he had an exfoliative dermatitis of his hands and feet, and some freckling on his face and shoulders. Collectively, these features support a diagnosis of ADULT syndrome. This study has identified a specific genotype-phenotype correlation in a rare ectodermal dysplasia syndrome and the findings are useful in improving genetic counselling in this family.

Base Sequence↗
PubMed1979

Anhidrotic ectodermal dysplasia with lacrimal anomalies.

Ectodermal dysplasia and its related disorders may present with ocular symptoms due to involvement of the ectodermal components of the eye. This paper reports a case of congenital anhidrotic ectodermal dysplasia presenting to the ophthalmologist with epiphora due to lacrimal atresia. The embryonic origin of the lacrimal system suggests that lacrimal anomalies in association with ectodermal disorders are commoner than reports indicate. Their management consists in accurate evaluation of the anomaly followed by surgery.

Child↗
PubMed1987

Autoneuralization in the amphibian ectoderm--a species-specific and stage-specific phenomenon.

Ectoderm from Ambystoma is especially prone to undergo 'autoneuralization'. This assertion has led to the maxim that ectoderm from this species is unsuitable for studying cell differentiation. Here we report that the degree of neuralization in cultured explants is stage-dependent. Control explants from blastulae (stage 8-9) show no neuralization, while explants treated with LiCl (10 mM) give rise to neuralization in about 70% of the cases. This difference between control and experiment decreases during gastrulation, in late gastrulae (stage 12) it is more or less negligible. Ectoderm from Cynops pyrrhogaster reacts like that of Ambystoma when exposed to LiCl, but like Triturus ectoderm it is insensitive to cyclic nucleotides.

Ambystoma↗
PubMed2002

Ectodermal dysplasia and brain cystic changes: confirmation of a novel neurocutaneous syndrome.

Ectodermal dysplasia is a rare congenital disorder characterized by dry, brittle hair, dental malformations, and skin abnormalities. It is thought to be the result of embryonic ectodermal dysgenesis, affecting tissues and structures that are widely separated but with common developmental origins. Recently, this disorder has been associated with a unique neuroimaging appearance, consisting of widely dilated perivascular spaces. This association has been proposed as a novel neurocutaneous syndrome, identified in one report as "cerebrum polycystica vera." We report a similar patient with dilated perivascular spaces associated with dermatologic manifestations consistent with ectodermal dysplasia. This patient was otherwise normal, without neurocognitive deficit. Additional neuroimaging findings included widespread white-matter high signal intensity on T2-weighted magnetic resonance imaging, as well as normal findings on magnetic resonance spectroscopy. This case confirms the association of ectodermal dysplasia and brain cystic changes and appears to expand the phenotypic manifestations that may be seen in such patients.

Brain↗
PubMed2005

Ectodermally derived steel/stem cell factor functions non-cell autonomously during primitive erythropoiesis in Xenopus.

Signals derived from nonhematopoietic tissues are essential for normal primitive erythropoiesis in vertebrates, but little is known about the nature of these signals. In Xenopus, unidentified factors secreted by ectodermal cells during gastrulation are required to enable the underlying ventral mesoderm to form blood. Steel is expressed in the ectoderm of early Xenopus embryos and is known to regulate definitive erythroid progenitor survival and differentiation in other organisms, making it an excellent candidate regulator of primitive erythropoiesis. In this study, we tested whether steel signaling is required for primitive red blood cell differentiation in mice and frogs. We show that Xsl is expressed in the ectoderm in Xenopus gastrulae and that c-kit homologs are expressed in the underlying mesoderm at the same stages of development. We present loss of function data in whole Xenopus embryos and explants that demonstrate a requirement for ectodermally derived steel to signal through c-kit in the mesoderm to support early steps in the differentiation of primitive erythroid but not myeloid cells. Finally, we show that primitive erythropoiesis is not disrupted in mouse embryos that lack c-kit function. Our data suggest a previously unrecognized and unique function of steel/c-kit during primitive erythropoiesis in Xenopus.

Animals↗
PubMed2003

X-linked anhidrotic ectodermal dysplasia (ED1) in men, mice, and cattle.

Ectodermal dysplasias are a large group of rare genetic disorders characterized by impaired development of hair, teeth, and eccrine glands in humans, mice, and cattle. Here, we review the cloning, mutation analyses, and functional studies of the known causative genes for the X-chromosomal anhidrotic ectodermal dysplasia (ED1) in these species. Mutations in the ectodysplasin 1 (ED1) gene are responsible for X-linked anhidrotic ectodermal dysplasia. The ED1 gene encodes a signaling molecule of the tumor necrosis factor family that is involved in development of ectodermal appendages. The bovine disorder may serve as an animal model for human ED1.

Animals↗
PubMed2004

Regionalisation of early head ectoderm is regulated by endoderm and prepatterns the orofacial epithelium.

The oral epithelium becomes regionalised proximodistally early in development, and this is reflected by the spatial expression of signalling molecules such as Fgf8 and Bmp4. This regionalisation is responsible for regulating the spatial expression of genes in the underlying mesenchyme. These genes are required for the spatial patterning of bone, cartilage orofacial development and, in mammals, teeth. The mechanism and timing of this important regionalisation during head epithelium development are not known. Using lipophilic dyes to fate map the oral epithelium in chick embryos, we show that the cells that will occupy the epithelium of the distal and the proximal mandible primordium already occupy different spatial locations in the developing head ectoderm prior to the formation of the first pharyngeal arch and neural crest migration. Moreover, the ectoderm cells fated to become proximal oral epithelium express Fgf8 and this expression requires the presence of endoderm. Thus, the first fundamental patterning process in jaw morphogenesis is controlled by the early separation of specific areas of ectoderm that are regulated by ectoderm-endoderm interactions, and does not involve neural crest cells.

Animals↗
PubMed2004

Distinct GATA6- and laminin-dependent mechanisms regulate endodermal and ectodermal embryonic stem cell fates.

This study investigates the establishment of alternative cell fates during embryoid body differentiation when ES cells diverge into two epithelia simulating the pre-gastrulation endoderm and ectoderm. We report that endoderm differentiation and endoderm-specific gene expression, such as expression of laminin 1 subunits, is controlled by GATA6 induced by FGF. Subsequently, differentiation of the non-polar primitive ectoderm into columnar epithelium of the epiblast is induced by laminin 1. Using GATA6 transformed Lamc1-null endoderm-like cells, we demonstrate that laminin 1 exhibited by the basement membrane induces epiblast differentiation and cavitation by cell-to-matrix/matrix-to-cell interactions that are similar to the in vivo crosstalk in the early embryo. Pharmacological and dominant-negative inhibitors reveal that the cell shape change of epiblast differentiation requires ROCK, the Rho kinase. We also show that pluripotent ES cells display laminin receptors; hence, these stem cells may serve as target for columnar ectoderm differentiation. Laminin is not bound by endoderm derivatives; therefore, the sub-endodermal basement membrane is anchored selectively to the ectoderm, conveying polarity to its assembly and to the differentiation induced by it. Unique to these interactions is their flow through two cell layers connected by laminin 1 and their involvement in the differentiation of two epithelia from the same stem cell pool: one into endoderm controlled by FGF and GATA6; and the other into epiblast regulated by laminin 1 and Rho kinase.

Basement Membrane↗
PubMed2005

Tsukushi controls ectodermal patterning and neural crest specification in Xenopus by direct regulation of BMP4 and X-delta-1 activity.

In Xenopus, ectodermal patterning depends on a mediolateral gradient of BMP signaling, higher in the epidermis and lower in the neuroectoderm. Neural crest cells are specified at the border between the neural plate and the epidermis, at intermediate levels of BMP signaling. We recently described a novel secreted protein, Tsukushi (TSK), which works as a BMP antagonist during chick gastrulation. Here, we report on the Xenopus TSK gene (X-TSK), and show that it is involved in neural crest specification. X-TSK expression accumulates after gastrulation at the anterior-lateral edges of the neural plate, including the presumptive neural crest region. In gain-of-function experiments, X-TSK can strongly enhance neural crest specification by the dorsolateral mesoderm or X-Wnt8 in ectodermal explants, while the electroporation of X-TSK mRNA in the lateral ectoderm of embryos after gastrulation can induce the expression of neural crest markers in vivo. By contrast, depletion of X-TSK in explants or embryos impairs neural crest specification. Similarly to its chick homolog, X-TSK works as a BMP antagonist by direct binding to BMP4. However, X-TSK can also indirectly regulate BMP4 mRNA expression at the neural plate border via modulation of the Delta-Notch signaling pathway. We show that X-TSK directly binds to the extracellular region of X-delta-1, and modulates Delta-dependent Notch activity. We propose that X-TSK plays a key role in neural crest formation by directly regulating BMP and Delta activities at the boundary between the neural and the non-neural ectoderm.

Animals↗
PubMed2006

Regulation of ectodermal Wnt6 expression by the neural tube is transduced by dermomyotomal Wnt11: a mechanism of dermomyotomal lip sustainment.

Ectodermal Wnt6 plays an important role during development of the somites and the lateral plate mesoderm. In the course of development, Wnt6 expression shows a dynamic pattern. At the level of the segmental plate and the epithelial somites, Wnt6 is expressed in the entire ectoderm overlying the neural tube, the paraxial mesoderm and the lateral plate mesoderm. With somite maturation, expression becomes restricted to the lateral ectoderm covering the ventrolateral lip of the dermomyotome and the lateral plate mesoderm. To study the regulation of Wnt6 expression, we have interfered with neighboring signaling pathways. We show that Wnt1 and Wnt3a signaling from the neural tube inhibit Wnt6 expression in the medial surface ectoderm via dermomyotomal Wnt11. We demonstrate that Wnt11 is an epithelialization factor acting on the medial dermomyotome, and present a model suggesting Wnt11 and Wnt6 as factors maintaining the epithelial nature of the dorsomedial and ventrolateral lips of the dermomyotome, respectively, during dermomyotomal growth.

Animals↗
PubMed2007

FoxI1e activates ectoderm formation and controls cell position in the Xenopus blastula.

The segregation of the vertebrate embryo into three primary germ layers is one of the earliest developmental decisions. In Xenopus, where the process is best understood, the endoderm is specified by a vegetally localized transcription factor, VegT, which releases nodal signals that specify the adjacent marginal zone of the blastula to become mesoderm. However, little is known about how the ectoderm becomes specified. In this paper, we show that the forkhead protein FoxI1e (also known as Xema) is required at the blastula stage for normal formation of both the central nervous system and epidermis, the two early derivatives of the ectoderm. In addition, FoxI1e is required to maintain the regional identity of the animal cells of the blastula, the cells that are precursors of ectodermal structures. In its absence, they lose contact with the animal cap, mix with cells of other germ layers and differentiate according to their new positions. Because FoxI1e is initially expressed in the animal region of the embryo and is rapidly downregulated in the neural plate, its role in neural and epidermal gene expression must precede the division of the ectoderm into neural and epidermal. The work also shows that FoxI1e plays a role in the embryo in the poorly understood process of differential adhesion, which limits cell mixing as primary germ layers become specified.

Animals↗
PubMed1988

Inductive effects of fibroblast growth factor and lithium ion on Xenopus blastula ectoderm.

We have studied the response of Xenopus blastula ectoderm to fibroblast growth factor and to lithium ion. The properties of acidic and basic FGF are very similar showing a 50% induction level at 1-2 ng ml-1 and a progressive increase of muscle formation up to concentrations of 100-200 ng ml-1. The elongation of explants also shows a dose-response relationship. The minimum contact requirement for induction of ectoderm explants is about 90 min and the stage range of ectodermal competence extends from midblastula to early gastrula, both these figures resembling those obtained in embryological experiments with vegetal tissue as the inducer. Lithium chloride concentrations which produce anteriorization of whole embryos have no effect on isolated ectoderms unless accompanied by FGF. Simultaneous treatment with FGF and Li lead to a marked enhancement of both elongation and muscle formation over that produced by FGF alone. By contrast, ventral marginal explants show increased elongation and muscle formation if treated with lithium alone suggesting that they have already received a low-dose FGF treatment within the embryo. It is concluded that endogenous FGF may be solely responsible for inducing the ventral mesoderm and that dorsalization of ventral mesoderm to the level of somitic muscle might be achieved either by a very high local concentration of FGF in the dorsal region, or by the action of a second, synergistic, agent in the dorsal region.

Animals↗
PubMed1990

Head morphogenesis in embryonic avian chimeras: evidence for a segmental pattern in the ectoderm corresponding to the neuromeres.

Areas of the superficial cephalic ectoderm, including or excluding the neural fold at the same level, were surgically removed from 3-somite chick embryos and replaced by their counterparts excised from a quail embryo at the same developmental stage. Strips of ectoderm corresponding to the presumptive branchial arches were delineated, thus defining anteroposterior 'segments' (designated here as 'ectomeres') that coincided with the spatial distribution of neural crest cells arising from the adjacent levels of the neural fold. This discrete ectodermal metamerisation parallels the segmentation of the hindbrain into rhombomeres. It seems, therefore, that not only is the neural crest patterned according to its rhombomeric origin but that the superficial ectoderm covering the branchial arches may be part of a larger developmental unit that includes the entire neurectoderm, i.e., the neural tube and the neural crest.

Animals↗