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PubMed1991

Protein kinase C and regulation of the local competence of Xenopus ectoderm.

The limited competence of embryonic tissue to respond to an inductive signal has an essential, regulatory function in embryonic induction. The molecular basis for the competence of Xenopus ectoderm to differentiate into neural tissue was investigated. Dorsal mesoderm or 12-O-tetradecanoyl phorbol-13-acetate (TPA) caused in vivo activation of protein kinase C (PKC) and neural differentiation mainly in dorsal ectoderm and to a lesser extent in ventral ectoderm. These data correlate with the observations that PKC preparations from dorsal and ventral ectoderm differ, the dorsal PKC preparation being more susceptible to activation by TPA and diolein than is the ventral PKC preparation. Monoclonal antibodies against the bovine PKC alpha plus beta or gamma isozymes immunostained dorsal and ventral ectoderm, respectively, which suggests different localizations of PKC isozymes. These results suggest that PKC participates in the establishment of embryonic competence.

Animals↗

PubMed2006

A mutation in the hair matrix and cuticle keratin KRTHB5 gene causes ectodermal dysplasia of hair and nail type.

BACKGROUND: Ectodermal dysplasias are developmental disorders affecting tissues of ectodermal origin. To date, four different types of ectodermal dysplasia involving only hair and nails have been described. In an effort to understand the molecular bases of this form of ectodermal dysplasia, large Pakistani consanguineous kindred with multiple affected individuals has been ascertained from a remote region in Pakistan. OBJECTIVE: To identify the gene underlying the phenotype. METHODS: Microsatellite markers were genotyped in candidate regions and two point and multipoint parametric linkage analysis carried out. RESULTS: The disease locus was mapped to a 16.6 centimorgan region on chromosome 12q12-q14.1 (Zmax = 8.2), which harbours six type II hair keratin genes. DNA sequence analysis revealed a homozygous missense mutation in the hair matrix and cuticle keratin KRTHB5, leading to histidine substitution of a conserved arginine residue (R78H) located in the head domain. CONCLUSIONS: This report provides the first direct evidence relating to the molecular pathogenesis of pure hair-nail ectodermal dysplasias.

Arginine↗

PubMed2004

Ectodysplasin A1 promotes placodal cell fate during early morphogenesis of ectodermal appendages.

Organs developing as appendages of the ectoderm are initiated from epithelial thickenings called placodes. Their formation is regulated by interactions between the ectoderm and underlying mesenchyme, and several signalling molecules have been implicated as activators or inhibitors of placode formation. Ectodysplasin (Eda) is a unique signalling molecule in the tumour necrosis factor family that, together with its receptor Edar, is necessary for normal development of ectodermal organs both in humans and mice. We have shown previously that overexpression of the Eda-A1 isoform in transgenic mice stimulates the formation of several ectodermal organs. In the present study, we have analysed the formation and morphology of placodes using in vivo and in vitro models in which both the timing and amount of Eda-A1 applied could be varied. The hair and tooth placodes of K14-Eda-A1 transgenic embryos were enlarged, and extra placodes developed from the dental lamina and mammary line. Exposure of embryonic skin to Eda-A1 recombinant protein in vitro stimulated the growth and fusion of placodes. However, it did not accelerate the initiation of the first wave of hair follicles giving rise to the guard hairs. Hence, the function of Eda-A1 appears to be downstream of the primary inductive signal required for placode initiation during skin patterning. Analysis of BrdU incorporation indicated that the formation of the epithelial thickening in early placodes does not involve increased cell proliferation and also that the positive effect of Eda-A1 on placode expansion is not a result of increased cell proliferation. Taken together, our results suggest that Eda-A1 signalling promotes placodal cell fate during early development of ectodermal organs.

Animals↗

PubMed2005

Neural crest determination by co-activation of Pax3 and Zic1 genes in Xenopus ectoderm.

A number of regulatory genes have been implicated in neural crest development. However, the molecular mechanism of how neural crest determination is initiated in the exact ectodermal location still remains elusive. Here, we show that the cooperative function of Pax3 and Zic1 determines the neural crest fate in the amphibian ectoderm. Pax3 and Zic1 are expressed in an overlapping manner in the presumptive neural crest area of the Xenopus gastrula, even prior to the onset of the expression of the early bona fide neural crest marker genes Foxd3 and Slug. Misexpression of both Pax3 and Zic1 together efficiently induces ectopic neural crest differentiation in the ventral ectoderm, whereas overexpression of either one of them only expands the expression of neural crest markers within the dorsolateral ectoderm. The induction of neural crest differentiation by Pax3 and Zic1 requires Wnt signaling. Loss-of-function studies in vivo and in the animal cap show that co-presence of Pax3 and Zic1 is essential for the initiation of neural crest differentiation. Thus, co-activation of Pax3 and Zic1, in concert with Wnt, plays a decisive role for early neural crest determination in the correct place of the Xenopus ectoderm.

Animals↗

PubMed2006

Specification of ectoderm restricts the size of the animal plate and patterns neurogenesis in sea urchin embryos.

The animal plate of the sea urchin embryo becomes the apical organ, a sensory structure of the larva. In the absence of vegetal signaling, an expanded and unpatterned apical organ forms. To investigate the signaling that restricts the size of the animal plate and patterns neurogenesis, we have expressed molecules that regulate specification of ectoderm in embryos and chimeras. Enhancing oral ectoderm suppresses serotonergic neuron differentiation, whereas enhancing aboral or ciliary band ectoderm increases differentiation of serotonergic neurons. In embryos in which vegetal signaling is blocked, Nodal expression does not reduce the size of the thickened animal plate; however, almost no neurons form. Expression of BMP in the absence of vegetal signaling also does not restrict the size of the animal plate, but abundant serotonergic neurons form. In chimeras in which vegetal signaling is blocked in the entire embryo, and one half of the embryo expresses Nodal, serotonergic neuron formation is suppressed in both halves. In similar chimeras in which vegetal signaling is blocked and one half of the embryo expresses Goosecoid (Gsc), serotonergic neurons form only in the half of the embryo not expressing Gsc. We propose that neurogenesis is specified by a maternal program that is restricted to the animal pole by signaling that is dependent on nuclearization of beta-catenin and specifies ciliary band ectoderm. Subsequently, neurogenesis in the animal plate is patterned by suppression of serotonergic neuron formation by Nodal. Like other metazoans, echinoderms appear to have a phase of neural development during which the specification of ectoderm restricts and patterns neurogenesis.

Animals↗

PubMed1989

Cutaneous nerves of the embryonic chick wing do not develop in regions denuded of ectoderm.

Peripheral nerves travel to their targets along precise routes, and it is likely that different cues provide guidance at different stages of the journey. In a developing chick limb, the cutaneous nerve fibres follow at first deep mixed nerve trunks, in company with motor axons; they branch from these trunks at predictable points and approach the skin; they then ramify profusely to form a plexus at a precisely defined depth beneath the ectoderm, at exactly the same level as the blood vascular plexus. To analyse the role of signals from the target patch of skin in regulating cutaneous nerve development, we have ablated patches of dorsal wing ectoderm using short-wave ultraviolet irradiation at E4 (embryonic day 4), approximately one day before nerves grow into the limb bud. The irradiated patches remain denuded of ectoderm for more than a week, by which time the cutaneous nerve plexus on the contralateral control side is well developed and can be revealed by whole-mount silver staining. Where the ectoderm has been ablated, no cutaneous nerve plexus forms, and the nerve branches that normally would have diverged from the neighbouring mixed nerve trunk to innervate the missing patch of skin are absent - ab initio, apparently. The routes of the mixed nerve trunks are not affected. Partial ablation of the territory of a cutaneous nerve branch often leads to loss of the whole nerve branch; the intact skin territory thus left vacant is invaded by ramifications from the remaining cutaneous branches, as expected if the normal extent of a cutaneous nerve's territory is regulated by competition. Where there is an ectodermal lesion, cutaneous innervation stops precisely at its boundary, even though the vascular plexus extends for some distance beyond this margin, beneath the denuded surface. The data suggest that the embryonic skin is required firstly to trigger divergence of cutaneous nerve branches from the mixed nerve trunks, and secondly, once the nerve fibres have reached the skin, to supply a trophic cue (probably NGF) encouraging growth of a plexus; at the same time, the embryonic skin generates a signal inhibiting nerves from approaching closer than about 70 microns to the surface.

Animals↗

PubMed1991

Hensen's node induces neural tissue in Xenopus ectoderm. Implications for the action of the organizer in neural induction.

The development of the vertebrate nervous system is initiated in amphibia by inductive interactions between ectoderm and a region of the embryo called the organizer. The organizer tissue in the dorsal lip of the blastopore of Xenopus and Hensen's node in chick embryos have similar neural inducing properties when transplanted into ectopic sites in their respective embryos. To begin to determine the nature of the inducing signals of the organizer and whether they are conserved across species we have examined the ability of Hensen's node to induce neural tissue in Xenopus ectoderm. We show that Hensen's node induces large amounts of neural tissue in Xenopus ectoderm. Neural induction proceeds in the absence of mesodermal differentiation and is accompanied by tissue movements which may reflect notoplate induction. The competence of the ectoderm to respond to Hensen's node extends much later in development than that to activin-A or to induction by vegetal cells, and parallels the extended competence to neural induction by axial mesoderm. The actions of activin-A and Hensen's node are further distinguished by their effects on lithium-treated ectoderm. These results suggest that neural induction can occur efficiently in response to inducing signals from organizer tissue arrested at a stage prior to gastrulation, and that such early interactions in the blastula may be an important component of neural induction in vertebrate embryos.

Activins↗

PubMed1992

Primary culture of single ectodermal precursors of Drosophila reveals a dorsoventral prepattern of intrinsic neurogenic and epidermogenic capabilities at the early gastrula stage.

We have analyzed the development in vitro of individual precursor cells from the presumptive truncal segmental ectoderm of the Drosophila embryo to study the intrinsic component in the determination of cell fate. For each cultured cell, the original position within as well as the developmental stage of the donor embryo were known. Cells removed from the ventral neurogenic region develop neural clones. Cells from the dorsal ectoderm and from the dorsalmost part of the ventral neurogenic ectoderm develop epidermal clones. These two classes of clones differ with respect to their division pattern, adhesiveness, cell morphologies and the expression of cell-specific markers. Mixed neural/epidermal clones were obtained from a fraction of precursors at almost all dorsoventral sites. We conclude that, at the onset of gastrulation, precursor cells of the truncal segmental ectoderm already have the capability to develop as either neuroblasts or epidermoblasts in the absence of further cell interactions. At the same time, positional cues distributed along the dorsoventral axis equip precursors with intrinsic preferences towards the neural or epidermal fate, thus defining a prepattern of high neurogenic preferences ventrally, and high epidermogenic preferences dorsally. It is likely that this prepattern is involved in defining the extent of the ventral neurogenic and dorsal epidermogenic regions of the ectoderm. The roles of intrinsic capabilities versus extrinsic influences in the regulation of the characteristic pattern of segregation of the two lineages are discussed.

Animals↗

PubMed1997

Neural tube-ectoderm interactions are required for trigeminal 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.

Animals↗

PubMed2006

Soft tissue facial angles in individuals with ectodermal dysplasia: A three-dimensional noninvasive study.

OBJECTIVE: To supply quantitative information about the facial soft tissues of patients with hypohidrotic ectodermal dysplasia. DESIGN: Prospective assessment. SETTING: National meetings of hypohidrotic ectodermal dysplasia patients and families. PATIENTS AND MAIN OUTCOME MEASURES: Facial and mandibular corpus convexities in the horizontal plane; facial convexity in the sagittal plane; interlabial, naso-labial, nasal convexity, and left and right soft tissue gonial angles were calculated from the three-dimensional coordinates of 11 soft tissue facial landmarks obtained in 18 male and 17 female hypohidrotic ectodermal dysplasia patients aged 3 to 41 years and in 504 reference healthy individuals. In addition, z-scores were computed and the patients were grouped by cluster analysis. RESULTS: Male and female z-scores did not differ. In the pooled group, facial convexities in the horizontal and sagittal planes were significantly (Student's t, p < .01) increased (flatter) in hypohidrotic ectodermal dysplasia patients, compared with normal controls. The naso-labial angle was significantly reduced (more acute). Upper and lower facial convexity and mandibular corpus convexity in the horizontal plane deviated less from the norm with increasing age. Facial convexity in the horizontal and sagittal planes, soft tissue gonial angles, and naso-labial and interlabial angles deviated less from the norm with increasing number of teeth present in the mouth. Cluster analysis identified three homogeneous groups, all characterized by a peculiar facial phenotype. Modifications in facial convexity and gonial and interlabial angles differentiated each cluster. CONCLUSIONS: Patients with hypohidrotic ectodermal dysplasia had flatter faces in the horizontal and sagittal planes than normal controls had. Cluster analysis revealed patterned differences in facial phenotype.

Adolescent↗

PubMed2002

[Hypohidrotic ectodermal dysplasia: A cause of fever of unknown origin].

The term ectodermal dysplasias includes many disorders that share some clinical features such as involvement of one or several ectodermal structures and congenital origin. Currently, 154 different types divided into 11 clinical subgroups (Freire Maia classification 1994) have been described. The most frequent entity is hypo- or anhidrotic ectodermal dysplasia (Christ-Siemens-Touraine syndrome). This is a rare hereditary disease whose main characteristic is the absence, or more often the reduction, of sweat glands, leading to an increase in body temperature together with anomalies of the epidermis and its appendages (hair and nails). We present a case of hypohidrotic ectodermal dysplasia in a premature 18-month-old boy who was referred to our department because of markedly dry skin since birth and recurrent eczematous and lichenification lesions that had been successfully treated with topical corticosteroids. Physical examination revealed mild alopecia with sparse and fine blonde hair and the absence of dental alveoli. The boy's mother had noticed slight sweating and episodes of fever without clinical symptoms, which were more frequent in summer. Hypohidrotic ectodermal dysplasia should be included in the differential diagnosis of fever of unknown origin.

Child, Preschool↗

PubMedDate not supplied

[The distribution of competence for adenohypophysis development in the ectoderm of chick embryos].

The ability of various zones of the cephalic and trunk ectoderm to differentiate into adenohypophysis after the contact with the bottom of the prosencephalon was studied in tissue culture of chick embryos as the stage of 10-13 somites. Stomodeal presumptive lens ectoderm and lateral cephalic ectoderms were shown to be competent for development into adenohypophysis. In all cases adenohypophyseal cords were formed in the zones of ectoderm contact with the brain. The cords contained antigens A-2, A-3 specific for chicken adenohypophysis as well as ACTH and beta-lopotropin. Trunk ectoderm proved to be incapable to differentiate into adenohypophysis.

Adrenocorticotropic Hormone↗

PubMedDate not supplied

[The determination of ectodermal derivatives in various species of amphibia].

The process of labyrinth determination has been studied in amphibians (three Urodela and seven Anura species) using homoplastic transplantation of ear ectoderm, containing labyrinth material onto the abdominal wall of embryos of the same stage of development. The stage of appearance of organ-specific properties in ear ectoderm was determined and the increase of these properties in the course of development was observed. The frequency of ear vesicles formation, the level of their differentiation and their size served as criteria. These criteria allow to align the studied species into a row, where organ-specific properties appear earlier and most completely in representatives of Ranidae family and in Bufo viridis, and weakest, in smooth newt. A comparison of properties of labyrinth material and other areas of ectoderm allowed to conclude that specific differences in determination of different ectodermal primordia are based on specific peculiarities of the whole ectoderm. The appearance of these differences can be explained by the shift in the beginning of gastrulation towards later stages of cleavage during the evolution of amphibians.

Amphibians↗

PubMed1977

[Morphogenesis of the chick embryo limb. Competence of the embryonic and extra-embryonic ectoderm].

Ecto-mesodermal interactions were investigated during the initiation of limb development in avian embryos. Experiments were performed on 2-day chick embryos. They consisted in implanting prospective leg mesoderm at different medio-lateral levels of the trunk and also into the extra-embryonic area. The implanted mesoderm was thus brought into contact with embryonic or extra-embryonic cicatricial or healing ectoderm, the ability of which to participate in the formation of an ectopic leg was tested. Whatever the level of embryonic ectoderm tested in hosts ranging from stage 14 to 27 pairs of somites (axial, paraxial, flank, ventrum), the experiments resulted in the formation of supernumerary limbs. Their frequency was level-dependent and decreased for each level, with increasing age of the host. The weakest competence was observed in the ectoderm of the prospective ventrum, the strongest in that of the prospective flank, axial and paraxial ectoderm showing an intermediary competence. Extra-embryonic ectoderm of blastoderms of the same age was unable to respond to the inducing action of the implanted prospective leg mesoderm. It was found to be incompetent, even at younger stages (5 to 13 pairs of somites).

Animals↗

PubMed1984

Development of the apical ectodermal ridge in the chick wing bud.

Histological examination of the stage-18 to stage-23 chick wing bud apex revealed the following. Initially, the wing bud was covered by a cuboidal to columnar epithelium with an overlying periderm. Thickening of the apical ectoderm was not obvious until late stage 18 (36 pairs of somites), after the appearance of the wing bud. At late stage 18, cells of the inner layer of ectoderm had elongated slightly along an axis perpendicular to the epithelial-mesenchymal interface. Well-defined apical ectodermal ridge morphology, i.e., pseudostratified columnar epithelium with an overlying periderm, was not apparent until stage 20. Subsequently the ridge lengthened along the anteroposterior perimeter of the wing bud. We demonstrated histologically that the apical ectodermal ridge of the wing bud was asymmetric with respect to the anteroposterior axis, in that there was more ridge associated with posterior mesoderm. Other observations include the spatial and temporal location of a groove in the base of the thickest part of the ridge. The groove can be correlated with the specification of distal wing elements. The groove was first seen at stage 20 and became more prominent through stage 23. An anteroposterior progression of ectodermal cell death was also observed. This began at late stage 18 and continued through each of the stages examined.

Animals↗

PubMed1981

Ectoderm-mesoderm interactions in relation to limb-bud chondrogenesis in the chick embryo: transfilter cultures and ultrastructural studies.

Limb ectoderm induces cartilage differentiation in mesoderm from chick embryo limb buds, Transfilter cultures have shown that this interactions requires 'contact' conditions and cannot take place at a distance. In vivo, a basement membrane is always present between ectoderm and mesoderm. The present paper demonstrates that the relationship between ectoderm and mesoderm is similar in vivo and in transfilter cultures. In culture conditions, the filter appears to be infiltrated by mesodermal cell outgrowths which form a continuous mesodermal cover on the filter. A basement membrane is always present between the mat of mesodermal cell processes and the ectoderm. Mesodermal cell processes are able to cross the Nuclepore filters (pore size 0.6-0.8 micrometer) within 15 min. After 2 h in culture, the surface of the filter opposite to the mesodermal explant is completely covered with mesodermal outgrowths. The extracellular material accumulating at the ectoderm-mesoderm interface appears to be mainly of mesodermal origin.

Animals↗

PubMed1995

Partially purified factor from embryonic chick brain can provoke neuralization of Rana temporaria and Triturus alpestris but not Xenopus laevis early gastrula ectoderm.

A high neuralizing activity has been determined in forebrain of 7.5-day old chick embryos using Rana temporaria early gastrula ectoderm as reacting tissue (Mikhailov and Gorgolyuk, Soviet Scientific Reviews, Section of Physiology and General Biology, Vol. 1: 267-306, 1987). The corresponding protease-sensitive agent was extracted, partially purified by chromatography on DEAE-Toyopearl and Heparin-Ultragel columns, and its neuralizing activity was tested in vitro on ectoderm isolated from early gastrulae of R. temporaria, Triturus alpestris, and Xenopus laevis at different concentrations and for different periods of time (animal cap assay). Induction of neural structures was found in R. temporaria and T. alpestris explants (up to 100 and 60%, respectively), but not in cultures of X. laevis ectoderm. Under our experimental conditions, so-called "autoneuralization" of the ectoderm explants can safely be excluded. The results are discussed in relation to the neural competence of amphibian ectoderm and the mechanisms of neuralizing actions of different factors which might be involved in neural induction and patterning.

Animals↗

PubMed1996

USF in the Lytechinus sea urchin embryo may act as a transcriptional repressor in non-aboral ectoderm cells for the cell lineage-specific expression of the LpS1 genes.

Expression of the aboral ectoderm-specific LpS1 gene in Lytechinus was used to study lineage-specific transcriptional regulation during sea urchin development. Band shift assays using anti-USF antibody showed that a USF-like protein bound the USF core sequence 5'-CACGTG-3' in the promoter of the LpS1 gene. DNA constructs consisting of a wild-type LpS1 promoter and the same LpS1 promoter with a mutated USF binding site fused to the bacterial chloramphenicol acetyltransferase reporter gene were tested. The mutation in the USF binding site caused an increase in chloramphenicol acetyltransferse activity. We selected a clone that encodes USF, LvUSF, from a gastrula-stage cDNA library representing Lytechinus variegatus. Transactivation experiments, in which LvUSF RNA or a DNA construct consisting of the LvUSF cDNA clone fused to the Lytechinus pictus metallothionein promoter coinjected with the wild-type or mutated LpS1 promoter-chloramphenicol acetyltransferase gene construct, showed that chloramphenicol acetyltransferase activity from the wild-type construct was repressed, while the construct mutated at the USF binding site was active. The same wild-type and mutated LpS1 promoter DNA fragments ligated to the green fluorescent protein reporter gene were used to examine spatial expression. The reporter gene constructs containing the mutated USF binding site were expressed inappropriately in all cell types including the gut and oral ectoderm in gastrula and larva stage embryos, while the wild-type constructs were expressed primarily in the aboral ectoderm. USF was expressed in all cells of the early embryo and in all tissues except the aboral ectoderm in later embryos. The data are consistent with a model depicting Lytechinus USF, as a temporal and spatial regulator by repressing LpS1 gene transcription in non-aboral ectoderm cells.

Amino Acid Sequence↗