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At least 109 records · Page 6Linked to original sources
PubMed2000

Regulative specification of ectoderm in skeleton disrupted sea urchin embryos treated with monoclonal antibody to Pl-nectin.

Pl-nectin is a glycoprotein first discovered in the extracellular matrix (ECM) of Paracentrotus lividus sea urchin embryo, apically located on ectoderm and endoderm cells. The molecule has been described as functioning as an adhesive substrate for embryonic cells and its contact to ectoderm cells is essential for correct skeletogenesis. The present study was undertaken to elucidate the biochemical characteristics of Pl-nectin and to extend knowledge on its in vivo biological function. Here it is shown that the binding of mesenchyme blastula cells to Pl-nectin-coated substrates was calcium dependent, and reached its optimum at 10 mM Ca2+. Perturbation studies using monoclonal antibody (McAb) to Pl-nectin, which prevent ectoderm cell-Pl-nectin contact, show that dorsoventral axis formation and ectoderm differentiation were retarded. At later stages, embryos recovered and, even if growth and patterning of the skeleton was greatly affected, the establishment of dorsoventral asymmetry was reached. Similarly, the expression of specific ectoderm and endoderm territorial markers was achieved, although occurring with some delay. Endoderm differentiation and patterning was not obviously affected. These results suggest that both endoderm and ectoderm cells have regulative capacities and differentiation of territories is restored after a lag period. On the contrary, failure of inductive differentiation of the skeleton cannot be rescued, even though the ectoderm has recovered.

Animals↗
PubMed2006

Dermatological manifestations of autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy syndrome.

BACKGROUND: Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy syndrome (APECED; OMIM 240300) is a rare autosomal recessive disorder defined by a variable combination of endocrine failure, chronic mucocutaneous candidiasis (CMC), and dystrophy of the dental enamel and nails. APECED is caused by mutations in the autoimmune regulator gene (AIRE). Alopecia areata (AA) and vitiligo are diseases with autoimmune pathogeneses, and have been recognized as part of the APECED complex. There are rare reports of other cutaneous manifestations. OBJECTIVES: We sought to delineate the dermatological features of APECED in an Irish case series with emphasis on timing of their appearance and association with disease severity. Furthermore, we looked for evidence of genotype: phenotype correlation. Finally, we wanted to determine if the ectodermal changes described represent a primary ectodermal dysplasia or whether the ectodermal manifestations are secondary phenomena. METHODS: Irish patients with APECED were invited to attend a multidisciplinary clinic (Dermatology, Endocrinology, Dentistry and Ophthalmology) held in Our Lady's Hospital for Sick Children, Dublin. Clinical data were compiled from case notes and questionnaires. All patients had a detailed cutaneous examination. Blood samples were obtained for mutational analysis. RESULTS: Eighteen patients (seven males and 11 females) from 15 families were interviewed and examined. The mean age at diagnosis was 6 years (range 8 months-18 years). All patients had evidence of CMC, 13 (72%) had candidal onychomycosis or paronychia, six (33%) had AA and two had vitiligo. In the case of two patients the diagnosis was made on recognition of dermatological manifestations and confirmed by mutational analysis. Both patients developed Addison's disease on follow-up. CMC was an early feature, often predating diagnosis (10 of 18). AA and vitiligo presented later, and may reflect more severe disease in these cases. There was no correlation between the AIRE mutations identified on mutational analysis and the clinical presentation. We found no evidence of an isolated nail dystrophy or features consistent with a primary ectodermal dysplasia. CONCLUSIONS: APECED is a rare but complex and potentially life-threatening autoimmune disease. CMC is a common and early feature; diagnosis at this stage may pre-empt life-threatening endocrinological crises. It is important for dermatologists to be aware of this association as they are likely to be the earliest clinicians who encounter these children. AA and vitiligo in our series occurred in the setting of established disease. The term "ectodermal dystrophy" is misleading as the ectodermal features described in our series and in the literature are most likely to be secondary phenomena.

Adolescent↗
PubMed1996

Expression of multiple CD44 isoforms in the apical ectodermal ridge of the embryonic mouse limb.

Previous immunohistochemical studies have shown that CD44 is highly enriched within the apical ectodermal ridge of the developing limb (Wheatley et al. [1993] Development 119: 295-306), but the particular isoforms of CD44 were not identified. We show here that CD44s (standard or "hemopoietic" isoform) and several CD44 variants, especially V3-V10, V4-V10, and V6-V10, are concentrated in the apical ectodermal ridge in the early mouse limb. Since CD44s is a major cell surface receptor for hyaluronan, we compared its localization with that of hyaluronan. In the early limb bud, hyaluronan is distributed throughout the mesoderm but is absent from all regions of the ectoderm. Hyaluronan is especially enriched in the basement membrane separating ectoderm and mesoderm, except beneath the apical ectodermal ridge where it is absent. Since CD44s is a known endocytic receptor for hyaluronan, its presence in ridge ectoderm could lead to degradation of hyaluronan destined for the neighboring region of basement membrane, thus facilitating interaction of the ridge with underlying mesoderm. The CD44 (V3-V10) isoform found in the ridge is expressed elsewhere as a proteoglycan with heparan sulfate chains that bind fibroblast growth factors. Since fibroblast growth factors are present in the ridge and are essential for limb morphogenesis, CD44 (V3-V10) is likely to act as a cofactor or modulator in the growth-promoting action or maintenance of the ridge.

Animals↗
PubMed1997

Epidermal ectoderm is required for full elevation and for convergence during bending of the avian neural plate.

Previous studies suggest that bending of the neural plate requires the juxtaposition of neural plate and non-neuroepithelial tissues. The current study examines the role of one of these tissues, the epidermal ectoderm, in bending. Chick blastoderms were harvested from fertile eggs incubated for 24 hr and cultured dorsal-side-up on agar-albumen substrates. In one experiment, a rectangular flap of epidermal ectoderm on one side of each blastoderm was separated from underlying layers and gently reflected onto the area opaca; a fragment of tungsten wire was placed on top of the flap to hold it down and to prevent healing. Embryos were then allowed to develop in a humidified incubator for 2-18 hr. Asymmetric neurulation was observed between the operated and control sides as early as 2 hr after surgery. The amount of asymmetry was quantified in serial transverse sections from embryos collected 8 hr after surgery. Elevation of the lateral edge of the neural plate on the operated side averaged one half to two thirds of that on the control side, and convergence of the operated side around the dorsolateral hinge point toward the dorsal midline did not occur. These results demonstrate that epidermal ectoderm is required for full elevation and for convergence during bending. In another experiment, lateral epidermal ectoderm was removed, leaving only a medial strip consisting of both the epidermal component of the future neural fold and flanking future epidermis. This experiment revealed that although epidermal ectoderm is necessary for full elevation and for convergence of the neural folds, a medial strip of epidermal ectoderm is sufficient to drive bending. Collectively, these results further support the idea that neurulation is a multifactorial process driven by both intrinsic and extrinsic factors acting in concert.

Animals↗
PubMed2000

Ectodermal markers delineate the neural fold interface during avian neurulation.

The formation and morphogenesis of the neural folds are important processes underlying neurulation. We showed previously that these processes comprise four key events in avian embryos: epithelial ridging, kinking, delamination, and apposition. Collectively, these events establish the paired, bilaminar neural folds, which fuse in the dorsal midline during late neurulation to close the neural groove and to establish the neural tube. Here, we use an antisense riboprobe for a new gene called Plato, as well as an antibody for a previously cloned transcription factor, AP-2, as markers to identify critical subpopulations of ectodermal cells during the formation and morphogenesis of the avian neural folds. Plato antisense riboprobe marks the cranial neural ectoderm and premigratory cranial neural crest cells, whereas AP-2 antibody marks the epidermal ectoderm and the early migratory neural crest. We show that subpopulations of ectodermal cells at the forebrain and midbrain levels undergo considerable rearrangement within the neural fold transition zone, which redistributes incipient neural crest cells from the neural ectodermal side of the forming neural fold interface to the epidermal ectodermal side. Additionally, we show that Plato and AP-2 provide useful markers for delineating the incipient neural fold interface.

Animals↗
PubMed2004

Ectodermal dysplasia with tetramelic deficiencies and no mutation in p63: odontotrichomelic syndrome or a new entity?

The ectodermal dysplasias (ED) are a large and complex group of diseases characterized by anomalies of the ectoderm and its derivates, often associated with malformations in other organs. We report a patient with an ectodermal dysplasia affecting hair, teeth, and nails and malformations of all four extremities including absence of several rays in the hands and feet. This patient shares many similarities with odontotrichomelic syndrome, a rare ectodermal dysplasia syndrome that has so far only been described in three individuals. However, some differences exist and this patient might also represent a separate ectodermal dysplasia syndrome. p63, a gene that is mutated in a number of syndromes associated with ectodermal dysplasia and limb malformations, was considered a possible candidate gene. However, no mutation in p63 was identified.

Adult↗
PubMed1993

Quantitative analysis of protein synthesis in mouse embryos. II: Differentiation of endoderm, mesoderm, and ectoderm.

The changes in protein synthesis that occur during differentiation of the primitive germ layers were examined by high-resolution, two-dimensional gel electrophoresis of proteins synthesized in 6.5 and 7.5 days postcoitum (d.p.c.) mouse embryos. For 6.5 d.p.c. embryos, protein synthesis patterns were compared between whole extraembryonic and embryonic regions and between embryonic visceral endoderm and embryonic ectoderm. For 7.5 d.p.c. embryos, comparisons were made between extraembryonic and embryonic regions and between isolated embryonic endoderm, mesoderm, and ectoderm. Each of the isolated 7.5 d.p.c. germ layers was divided into anterior and posterior fragments in order to evaluate possible regional differences in gene expression along the anterior-posterior axis. Comparisons of protein synthesis patterns revealed the greatest difference between isolated endoderm and ectoderm, indicating that by as early as 6.5 d.p.c. patterns of gene expression differ significantly between these tissues. The greatest similarities were found between ectoderm and whole embryonic regions and between endoderm and whole extraembryonic regions, which most likely reflects the overall cellular compositions of the embryonic and extraembryonic regions. Based on their patterns of synthesis, four groups of proteins were identified that were preferentially synthesized in either endoderm or ectoderm. These provide useful markers for studying differentiation in these tissues. One other protein, migrating at the position expected for vimentin, was synthesized at an elevated rate in isolated mesoderm. We also observed differences in rates of synthesis of alpha-tubulin and tropomyosin-5 indicative of potential differences in cytoskeletal composition among the germ layers beyond those previously described. The difference in overall protein synthesis patterns between anterior and posterior regions was greatest in the embryonic endoderm, indicating that differentiation along the anterior-posterior axis may be initiated sooner or may proceed more rapidly in the endoderm than in the other germ layers. These data provide the first quantitative evaluation of the degree to which differentiation of the three primitive germ layers affects protein synthesis patterns and reveal potentially useful markers of endoderm and ectoderm differentiation.

Animals↗
PubMed1994

Pax-6 is first expressed in a region of ectoderm anterior to the early neural plate: implications for stepwise determination of the lens.

The Pax-6 gene encodes a DNA-binding transcription factor essential to normal development of the mammalian eye. We have found that in the chick embryo, the Pax-6 gene is first expressed in a crescent-shaped region of future head ectoderm that adjoins the anterior margin of the early neural plate. As development proceeds, this region of Pax-6-positive ectoderm becomes divided into two bilateral domains. Upon contact with the optic vesicles, portions of these domains give rise to the invaginating lens placodes, which contain high levels of Pax-6 mRNA. As with mouse, rat, and zebrafish, chick Pax-6 is also expressed in the neural epithelium of the forebrain and optic vesicles. However, our results indicate that the onset of expression in the prospective head ectoderm occurs at a substantially earlier stage. Experiments involving unilateral ablation of the anterior neural plate indicate that contact with an optic vesicle is not required to maintain expression of Pax-6 in the ectoderm. Experiments in which optic vesicles have been displaced from their normal location further suggest that positioning of Pax-6 domains in the head ectoderm is independent of neighboring optic vesicles. Homozygous defects in the mouse and rat Pax-6 gene are known to cause complete failure of lens formation at the optic vesicle stage and block subsequent development of the optic cup. Our results raise the possibility that Pax-6 may be involved in the early establishment of lens-competent regions within the head ectoderm.

Amino Acid Sequence↗
PubMed1995

Ectoderm-mesenchyme and mesenchyme-mesenchyme interactions regulate Msx-1 expression and cellular differentiation in the murine limb bud.

The apical ectodermal ridge (AER) is a specialized thickening of the distal limb mesenchyme that has been demonstrated to support limb outgrowth and proper limb development. The homeobox gene, Msx-1, is associated with the distal limb mesenchyme (progress zone) and its expression depends upon the presence of the AER in chick limbs. We demonstrate here that the expression of Msx-1 is dependent upon the limb ectoderm in the mouse, but that the inductive capacity of murine limb ectoderm is not restricted to the AER. Msx-1 can also be maintained in limb mesenchyme by the substitution of FGF 4 for the ectoderm; however, we see that local cell-cell interactions are required for high levels of expression. Disruption of cell-cell interactions in the limb mesenchyme results in a dramatic decrease in Msx-1 levels and a precocious expression of MyoD1, suggesting that the limb environment represses differentiation and promotes cell proliferation during early development. BMP 4 and FGF 2 can also maintain Msx-1 expression in limb mesenchyme as well as retinoic acid which is usually associated with polarizing activity in the early limb. Msx-2 expression does not appear to be dependent upon cell-cell interactions as measured in these experiments. Taken together, our data suggest that the expression of Msx-1, but not Msx-2, not only requires factors from the limb ectoderm, but also relies upon cues from local cell interactions and that the spatial distribution of inductive capacities in limb ectoderm differs between the avian and murine systems.

Animals↗
PubMed1995

The matured eye of Xenopus laevis tadpoles produces factors that elicit a lens-forming response in embryonic ectoderm.

Previous studies have indicated that the outer cornea can undergo transdifferentiation to form a lens in the tadpole larva of Xenopus laevis following removal of the original lens. This transformation appears to require an interaction with the neural retina. In the present study, we carried out a series of experiments to determine if the matured tadpole eye can also elicit lens formation in embryonic ectoderm. Labeled embryonic ectoderm was removed from the presumptive lens-forming region, or from the belly region (ventral ectoderm), at various stages of development (stages 11-19, gastrula to neural tube stages) and implanted into the eye cavity (posterior chamber) of advanced stage 52-55 tadpoles. After 3 days, we examined the tadpoles and their implanted tissues for lens cell formation using lens-specific antibodies. Implanted presumptive lens ectoderm differentiated lens cells in a large number of cases. The percentage of cases forming lens cells and the extent of morphological differentiation increased with increasing age of the implanted tissue. Implanted ventral ectoderm also formed lens cells, although at a reduced frequency and with limited morphological differentiation. These results indicate that the environment of the matured tadpole eye cavity stimulates lens cell formation in both presumptive lens and nonlens ectoderm. The development of the implanted tissues was compared to that found in previous studies where these tissues were cultured as explants or transplanted to lens-forming regions during early development and subjected to various periods of embryonic lens induction. Together, these findings suggest that the process of embryonic lens formation is related to that involved in transdifferentiation of the tadpole cornea during "lens regeneration." However, the inductive effect of the matured tadpole eye is qualitatively different from that of the early period of embryonic lens induction and, while more intense, may be more closely related to that which takes place via the optic vesicle during the later phase of embryonic lens induction.

Animals↗
PubMed2002

Ectodermal FGFs induce perinodular inhibition of limb chondrogenesis in vitro and in vivo via FGF receptor 2.

The formation of cartilage elements in the developing vertebrate limb, where they serve as primordia for the appendicular skeleton, is preceded by the appearance of discrete cellular condensations. Control of the size and spacing of these condensations is a key aspect of skeletal pattern formation. Limb bud cell cultures grown in the absence of ectoderm formed continuous sheet-like masses of cartilage. With the inclusion of ectoderm, these cultures produced one or more cartilage nodules surrounded by zones of noncartilaginous mesenchyme. Ectodermal fibroblast growth factors (FGF2 and FGF8), but not a mesodermal FGF (FGF7), substituted for ectoderm in inhibiting chondrogenic gene expression, with some combinations of the two ectodermal factors leading to well-spaced cartilage nodules of relatively uniform size. Treatment of cultures with SU5402, an inhibitor FGF receptor tyrosine kinase activity, rendered FGFs ineffective in inducing perinodular inhibition. Inhibition of production of FGF receptor 2 (FGFR2) by transfection of wing and leg cell cultures with antisense oligodeoxynucleotides blocked appearance of ectoderm- or FGF-induced zones of perinodular inhibition of chondrogenesis and, when introduced into the limb buds of developing embryos, led to shorter, thicker, and fused cartilage elements. Because FGFR2 is expressed mainly at sites of precartilage condensation during limb development in vivo and in vitro, these results suggest that activation of FGFR2 by FGFs during development elicits a lateral inhibitor of chondrogenesis that limits the expansion of developing skeletal elements.

Animals↗
PubMed1995

Experimental analyses of the rearrangement of ectodermal cells during gastrulation and neurulation in avian embryos.

The rearrangement of ectodermal cells was studied in chimeras in which grafts were transplanted during late gastrula and early neurula stages to heterotopic locations in avian embryos. Three types of experiments were done. In all experiments, Hensen's node was extirpated completely and replaced with an epithelial plug derived from 1 of 3 regions of the prospective ectoderm. In type-1 experiments, Hensen's node was replaced with a plug consisting of precursor cells of the floor plate of the neural tube. In type-2 experiments, Hensen's node was replaced with a plug consisting of precursor cells of the lateral wall of the neural tube. In type-3 experiments, Hensen's node was replaced with a plug consisting of precursor cells of the epidermal ectoderm. In all experiments, the amount and direction of cell rearrangement that occurred in the transplanted ectodermal plug was essentially typical for prospective ectodermal cells normally residing within Hensen's node. That is, transplanted ectodermal cells underwent lateral-to-medial cell-cell intercalation and contributed to the ventral midline of the neural tube along its entire rostrocaudal extent. In most embryos, a notochord was reconstituted from host cells, despite the fact that Hensen's node--the prime source of prospective notochordal cells in intact embryos--was extirpated completely; however, a few embryos had long notochordal gaps. In such essentially notochordless embryos, the ventral midline of the neural tube still derived from grafted cells, but it failed to form a floor plate, providing further confirmation of the results of several previous studies that the notochord is required to induce the floor plate.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Ocular symptoms and signs in patients with ectodermal dysplasia syndromes.

PURPOSE: The ectodermal dysplasia syndromes are underestimated although precise inclusion criteria have been formulated. The purpose is to establish easily detectable ophthalmologic symptoms and signs as reliable criteria for ectodermal dysplasia syndromes. METHODS: Thirty-six patients with confirmed ectodermal dysplasia syndromes were included in an observational case series: hypohidrotic ectodermal dysplasia (30), EEC syndrome (3), AEC syndrome (2), Gorlin-Goltz syndrome (1). Each patient was examined ophthalmologically. The principal outcome measures were ocular symptoms and signs in patients with different ectodermal dysplasia syndromes of varying severity. METHODS: Some 94.4% of the patients suffered from dry eye symptoms. Reduction of eyebrows was seen in 94.4%; the lashes were altered in 91.6%. Changes of the meibomian glands were detected in 95.45%. Corneal changes such as pannus occurred later in life. CONCLUSIONS: Alterations of the meibomian glands, which were detected by meibomianoscopy, are the most reliable ocular sign of ectodermal dysplasia syndromes.

Adolescent↗
PubMed2001

The apical ectodermal ridge, fibroblast growth factors (FGF-2 and FGF-4) and insulin-like growth factor I (IGF-I) control the migration of epidermal melanoblasts in chicken wing buds.

The role of the apical ectodermal ridge and of fibroblast growth factors FGF-2 and FGF-4 and of the insulin-like growth factor I (IGF-I) in the control of the migration of epidermal melanoblasts was investigated using quail-chicken chimeras. Wing buds of a strain of unpigmented chicken were microsurgically modified in several ways (ablation, displacement or implantation of additional apical ectodermal ridges, implantation of grafts devoid of apical ectodermal ridges, ectopic application of growth factors) and received grafts containing quail neural crest cells. The distribution of the epidermal melanoblasts which had differentiated from the quail grafts revealed that both the apical ectodermal ridge and the growth factors invariably caused the migration of epidermal melanoblasts towards them. This leads to the conclusion that the presence of the apical ectodermal ridge is the sufficient condition to direct the migration of epidermal melanoblasts within the avian embryonic wing bud. Furthermore, FGF-2 and IGF-I and to a lesser extent FGF-4 play a decisive role in directing the migration of epidermal melanoblasts within chicken wing buds and are likely to be involved in the molecular cascade by means of which the apical ectodermal ridge controls the migration of epidermal melanoblasts.

Animals↗
PubMed1986

Experimental manipulation leading to induction of dorsal ectodermal ridges on normal limb buds results in a phenocopy of the Eudiplopodia chick mutant.

Elongation of chick limb buds depends on the presence of the apical ectodermal ridge which is induced by subjacent limb bud mesoderm. Recombination experiments have shown that the limb bud mesoderm loses the capacity to induce ridges by late stage 17. Moreover, in normal limb development only one ridge forms. However, in the eudiplopodia chick mutant accessory ectodermal ridges form on the dorsal surface of limb buds as late as stage 22. Tissue recombinant experiments show that the mutation affects the ectoderm, extending the time it responds to ridge induction (R.A. Fraser and U.K. Abbott (1971). J. Exp. Zool. 176, 237-248) while the mesoderm is normal. The result is polydactyly, with extra digits dorsal to the normal digits. Because eudiplopodia limb bud dorsal mesoderm can induce ridges at stage 22 but is unaffected by the gene, genetically normal dorsal limb bud mesoderm may also be able to induce ridges after stage 17. To test this possibility we grafted stages 14-18 flank ectoderm to normal limb bud dorsal mesoderm and found that mesoderm from stages 17 through 20 was able to induce a ridge and subsequently dorsal digits developed. Limbs with duplicate digits were similar to eudiplopodia limbs. In other experiments, stage 18, 19, and 20 leg bud dorsal ectoderm did not form ridges when grafted to leg bud dorsal mesoderm of the same stage, indicating a lack of response to the mesoderm. Finally, the inductive capacity of limb bud mesoderm appeared to be reduced compared to mesoderm at pre-limb bud stages. These experiments demonstrate a spatially generalized potential in limb bud dorsal mesoderm to induce ridges during the stages when the apical ridge is induced. The determination of where the ridge will form and the acquired inability of limb bud dorsal ectoderm to respond to induction by underlying mesoderm are necessary early pattern forming events which assure that a single proximodistal limb axis will form.

Animals↗
PubMed1986

Normal development of the skeleton in chick limb buds devoid of dorsal ectoderm.

It has been suggested that the ectoderm on the dorsal and ventral faces of the limb bud plays a part in controlling the pattern of cartilage differentiation. To test this, the dorsal wing bud ectoderm in the chick embryo was destroyed by irradiation with ultraviolet light at stage 17-19, at the very beginning of limb bud development, but the apical ectodermal ridge was spared. The irradiated ectoderm disappeared within 24 hr (by stage 23-24) and did not regenerate thereafter; thus the dorsal surface of the limb bud was kept denuded throughout most of the period of skeletal pattern formation. By 6 or 7 days after the irradiation (stage 35), when the rudiments of all the adult skeletal elements are normally present in recognizable form, the irradiated wings could be placed into two categories, those that were approximately normal in shape and those that had curled dorsally. All of these limbs were reduced in size, to varying degrees, when compared to their controls and lacked dorsal soft tissues. The limbs that were normal in shape, however, even though sometimes denuded over practically the whole extent of their dorsal surface, almost always had a complete and normally proportioned cartilage pattern, suggesting that ectoderm (other than the apical ectodermal ridge) does not exert any direct control over the development of the limb cartilage pattern. However, many of those limbs that had curled as a result of the irradiation did have major pattern deformities, suggesting that the topology of cartilage differentiation does depend on the shape of the limb bud.

Animals↗
PubMed1987

Inductive interactions in the spatial and temporal restriction of lens-forming potential in embryonic ectoderm of Xenopus laevis.

The process of lens cell determination in amphibians is currently viewed as one involving a series of inductive interactions. On the basis of previous investigations, these interactions are thought to begin during gastrulation when the presumptive foregut endoderm and then the heart mesoderm come into contact with the presumptive lens ectoderm. This earlier period of induction is followed by the later interaction of the optic vesicle with the lens-forming ectoderm. Transplantation experiments were performed to determine the relative significance of the early and later periods of induction in the process of lens cell determination in the anuran Xenopus laevis. Various ectodermal tissues were transplanted either into the lens-forming region of open neural plate stage host embryos or over the newly formed optic vesicle of later neurula stage embryos. All transplanted tissues were labeled with the intracellular marker horseradish peroxidase to assess the exact origins of any induced lens structures. The results indicate that all nonneural ectodermal tissues have some lens-forming potential early during gastrulation; however, this potential is restricted to the lens-forming region, and perhaps nearby regions, later in development during the time of neurulation. Furthermore, the results show that the optic vesicle is not a substantial inductor of the lens in tissues that have not been previously exposed to the earlier series of inductive interactions that take place during gastrulation and neurulation. Since the optic vesicle does not appear to be a sufficient inductor of the lens, these earlier inductive interactions are, therefore, essential in the process of lens cell determination in Xenopus. These earlier inductive interactions lead to a steady increase in what may be called a lens-forming bias in the presumptive lens ectoderm during this period of development. The eventual loss in the ability of nonlens ventral ectoderm to respond to these lens inductors is presumably the result of other determinative processes that occur in this tissue.

Animals↗
PubMed1991

Removal of N-linked oligosaccharides of presumptive ectoderm impairs neural induction in Pleurodeles waltl.

Studies were carried out on the embryo of the amphibian Pleurodeles waltl to investigate the potential role of the N-linked oligosaccharides of the ectodermal cell membrane in the neural induction process. Glycopeptidase F (GPase F) was used to cleave N-linked oligosaccharides on presumptive ectoderm. Removal of oligosaccharide moieties from ectoderm membrane glycoconjugates completely inhibited natural neural induction in vitro. On the other hand, Swainsonine (Sw) and 1-deoxynojirimycin (dNM), specific inhibitors of enzymes involved in glycosylation, provoked strong and persistent changes in the structure of the N-linked oligosaccharides of presumptive ectoderm but did not prevent neuralisation of treated ectoderm. We conclude that N-linked carbohydrates are implicated in the phenomenon of neural induction. However, the structural integrity of N-linked carbohydrates of target tissue is not itself critical in this process. The existence of specific carbohydrates on presumptive ectoderm was still questioned as receptors of neural signal.

1-Deoxynojirimycin↗