SEARCH · Search PubMed

Results for “ECTODERM”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 451 records · Page 25Linked to original sources

PubMed2003

Child with De Novo t(1;6)(p22.1;p22.1) translocation and features of ectodermal dysplasia with hypodontia and developmental delay.

We report on a 6.5-year-old girl with a balanced translocation between the short arms of chromosomes 1 and 6. She was referred for genetics evaluation because of developmental speech delay and congenital absence of several deciduous and permanent teeth. She was very sensitive to noise (hyperacusis), had poor hair and nail growth, decreased sweating, and turned very red with high fever. She had microcephaly (head circumference at the second centile; weight and height were at 25th centile), short palpebral fissures, epicanthal folds, sparse eyelashes, large ears, partial anodontia, short finger and toenails, and dry skin. She had mild developmental delay. Family history was significant for learning problems in two paternal uncles, one paternal aunt, and several paternal cousins. Thyroid studies, calcium, phosphorus, and alkaline phosphatase levels were normal. Her karyotype was 46,XX,t(1;6)(p22.1;p22.2), and parental karyotypes were normal. This apparently balanced translocation may have resulted in either a submicroscopic loss or disruption of a gene or genes involved in ectodermal dysplasia. There are no reported cases of ectodermal dysplasia associated with this chromosome rearrangement.

Anodontia↗

PubMed2004

Hypertelorism, ptosis, and myopia associated with drug-resistant epilepsy, mental delay, growth deficiency, ectodermal defects, and osteopenia.

We report a 30-year-old woman with hypertelorism, ptosis, and myopia associated with drug-resistant epilepsy (DRE, Lennox-Gastaut syndrome), mental delay, growth deficiency, ectodermal defects, and osteopenia. To the best of our knowledge, this patient has an unusual combination of symptoms not previously described, associated with severe central nervous system dysfunction. The ectodermal defects were present in a very intriguing form, were difficult to diagnose, and did not conform to any classification or previous description.

Adult↗

PubMed1994

Domains of differential cell proliferation and formation of amnion folds in chick embryo ectoderm.

Patterns of cell proliferation in ectoderm epithelium that will form avian amnion correlate with morphogenesis, but not in an obvious pattern with respect to large-scale folding. At sites where the pre-axial amnion folds will first appear in 4- to 8-somite embryos, patterns of proliferation do not separate into domains that presage location of the single pre-axial fold that is commonly described in embryology texts. Instead, increased cell proliferation occurs in a significant, bilateral pattern. In stages with 13 to 27 somites, when lateral amnionic folds are prominent, five paraxial domains of cell proliferation correlate with morphology and show decreasing levels of cell proliferation with distance from the neural axis. Slowly growing areas surround rapidly growing areas and could assist buckling of epithelium by providing constraints on expansion of faster growing areas. Proliferation domains in ectoderm correlate with morphology and morphological events when localized changes in cell shape are lacking and suggest a role for differential cell proliferation in formation of large-scale epithelial folds in early chick embryos.

Amnion↗

PubMed2001

Regulation of Epha4 expression in paraxial and lateral plate mesoderm by ectoderm-derived signals.

Somitogenesis in all vertebrates involves a mesenchymal to epithelial transition of segmental plate cells. Such a transition involves cells altering their morphology and their adhesive properties. The Eph family of receptor tyrosine kinases has been postulated to regulate cytoskeletal organization. In this study, we show that a receptor belonging to this family, EphA4, is expressed in the segmental plate in a region where cells are undergoing changes in cell shape as a prelude to epithelialization. We have identified the ectoderm covering the somites and the midline ectoderm as sources of signals capable of inducing EphA4. Loss of EphA4 results in cells of irregular morphology and somites fail to form. We also show that when somites fail to develop, expression of EphA4 in the lateral plate is also lost. We suggest that signaling occurs between the somites and the lateral plate mesoderm and provide evidence that retinoic acid is involved in this communication.

Animals↗

PubMed2005

Notch1 signals through Jagged2 to regulate apoptosis in the apical ectodermal ridge of the developing limb bud.

The Notch family of receptors is involved in a wide variety of developmental processes, including cell fate specification, cell proliferation, and cell survival decisions during cell differentiation and tissue morphogenesis. Notch1 and Notch ligands are expressed in the developing limbs, and Notch signalling has been implicated in the formation of a variety of tissues that comprise the limb, such as the skeleton, musculature, and vasculature. Notch signalling has also been implicated in regulating overall limb size. We have used a conditional allele of Notch1 in combination with two different Cre transgenic lines to delete Notch1 function either in the limb mesenchyme or in the apical ectodermal ridge (AER) and limb ectoderm. We demonstrate that Notch signalling, involving Notch1 and Jagged2, is required to regulate the number of Fgf8-expressing cells that comprise the AER and that regulation of the levels of fibroblast growth factor signalling is important for the freeing of the digits during normal limb formation. Regulation of the extent of the AER is achieved by Notch signalling positively regulating apoptosis in the AER. We also demonstrate that Notch1 is not required for proper formation of all the derivatives of the limb mesenchyme.

Animals↗

PubMed1989

Molecular genetics of Delta, a locus required for ectodermal differentiation in Drosophila.

Delta (Dl) is one of the six known zygotic neurogenic genes, each of which is essential for proper segregation of the embryonic ectoderm into neural and epidermal lineages. Molecular analysis of Dl reveals that it is a transcriptionally complex locus that yields multiple maternal and zygotic transcripts. DNA sequence analysis suggests that the predominant product of the locus is a putative transmembrane protein exhibiting homology to blood coagulation factors and epidermal growth factor of vertebrates. The structure of this product is consistent with the hypothesis that Dl participates in cell-cell interactions that are central to establishment of the epidermal lineage within the developing ectoderm. Genetic analyses demonstrate that Dl mutations can modify the imaginal phenotypes that result from heterozygosity for Notch (N) mutations as well as the interaction between particular alleles of Notch (N) and Enhancer of split [E(spl)], two other members of the neurogenic gene set. Vital interactions also occur between Dl and N. Given the structures of products encoded by N, Dl, and E(spl), we suggest that the synergistic phenotypic interactions observed among mutations in these three loci result from physical, as opposed to regulatory, interactions.

Alleles↗

PubMed1990

Fate mapping the avian epiblast with focal injections of a fluorescent-histochemical marker: ectodermal derivatives.

A microinjection technique is described for fate mapping the epiblast of avian embryos. It consists of injecting the epiblast of cultured blastoderms with a fluorescent-histochemical marker, examining rhodamine fluorescence at the time of injection in living blastoderms, and assaying for horseradish peroxidase activity in histological sections obtained from the same embryos collected 24 h postinjection. Our results demonstrate that this procedure routinely marks cells, allowing their fates to be determined and prospective fate maps to be constructed. Two such maps are presented for ectodermal derivatives of the epiblast: one for late stages of Hensen's node progression (stages 3c through 4) and one for early stages of node regression (stages 4 + through 5). These new maps have six significant features. First, they show that regardless of whether the node is progressing or regressing, the flat neural plate extends at least 300 microns cranial to, 300 microns bilateral to and 1 mm caudal to the center of Hensen's node. Second, they confirm our previous fate mapping studies based on quail/chick chimeras. Namely, they show that the prenodal midline region of the epiblast forms the floor of the forebrain and the ventrolateral part of the optic vesicles as well as MHP cells (i.e., mainly wedge-shaped neurepithelial cells contained within the median hinge point of the bending neural plate); in contrast, paranodal and postnodal regions contribute L cells (i.e., mainly spindle-shaped neurepithelial cells constituting the lateral aspects of the neural plate). Third, they reveal a second source of MHP cells, Hensen's node, verifying previous studies of others based on tritiated thymidine labeling. Fourth, they demonstrate, in contrast to studies of other based on vital staining, carbon marking, and chorioallantoic grafting but in accordance with our previous studies based on quail/chick chimeras, that the cells contributing to the four craniocaudal subdivisions of the neural tube (i.e., forebrain, midbrain, hindbrain, and spinal cord) are not yet spatially segregated from one another at the flat neural plate stage, although more cranial neural plate cells tend to form more cranial subdivision and more caudal cells tend to form more caudal subdivisions. Thus, single injections routinely mark multiple neural tube subdivisions. Probable reasons for the discrepancy between our present results and the previous results of others is discussed. Fifth, they suggest that cells contributing to the surface ectoderm and neural plate are not yet completely spatially segregated from one another at the flat neural plate stage, particularly in caudal postnodal regions. Sixth, they delineate the locations of the otic placodes.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2002

Adult bone marrow stromal stem cells express germline, ectodermal, endodermal, and mesodermal genes prior to neurogenesis.

Bone marrow stromal stem cells (MSCs) normally differentiate into mesenchymal derivatives but recently have also been converted into neurons, classical ectodermal cells. To begin defining underlying mechanisms, we extended our characterization of MSCs and the differentiated neurons. In addition to expected mesodermal mRNAs, populations and clonal lines of MSCs expressed germinal, endodermal, and ectodermal genes. Thus, the MSCs are apparently "multidifferentiated" in addition to being multipotent. Conversely, the differentiating neurons derived from populations and clonal lines of MSCs expressed the specific markers beta-III tubulin, tau, neurofilament-M, TOAD-64, and synaptophysin de novo. The transmitter enzymes tyrosine hydroxylase and choline acetyltransferase were localized to neuronal subpopulations. Our observations suggest that MSCs are already multidifferentiated and that neural differentiation comprises quantitative modulation of gene expression rather than simple on-off switching of neural-specific genes.

Age Factors↗

PubMed2006

Long-term cryopreserved amniocytes retain proliferative capacity and differentiate to ectodermal and mesodermal derivatives in vitro.

Putative stem cells have recently been isolated from several extra-embryonic tissues, including Wharton's Jelly and umbilical cord blood. Relevant studies have focused on primary cultures established from freshly isolated tissues. In this report, we examine the plasticity of 472 cells, a cryopreserved human amniocyte cell line originally isolated in 1974. Under conditions conducive for proliferation, the amniocytes displayed fibroblast-like morphologies and expressed Oct4 and Rex1, genes associated with pluripotency. Perhaps indicative of inherent plasticity, 472 cells simultaneously expressed ectodermal beta-III-tubulin and mesodermal fibronectin. When cultured under conditions that promote neural differentiation, the cells adopted neuronal morphologies and expressed neuronal genes, including Gap-43, NF-M, tau, and synaptophysin. Exposure to culture conditions that encourage osteogenic differentiation resulted in increased expression of alkaline phosphatase (ALP) and the deposition of mineralized matrix, established markers of bone cell differentiation. In sum, this population of human amniocytes appears to be multipotent, capable of in vitro differentiation to ectodermal and mesodermal cell types. Retention of this plasticity through decades of cryopreservation suggests that amniocytes might be candidates for future cell-based therapies.

Amnion↗

PubMed1975

The community of human malformation syndromes that shares ectodermal dysplasia and deformities of the hands and feet.

Syndromes of human congenital malformation may be classified be recognizing communities of syndromes that share multiple phenotypic similarities involving their principal diagnostic features. A community of syndromes that shares various expressions of ectodermal dysplasia and various deformities of the hands and feet is proposed; these syndromes are divisible into two classes according to the presence or absence of anomalies in the nasal or labial regions of the face. The dysmorphogenetic validity of the division is supported by the fact that the syndromes without nasal or labial anomalies have a high frequency of sensorineural deafness as one expression of ectodermal dysplasia whereas those without such anomalies do not. The usefulness of such a syndromal community as a base for evolving a taxonomic scheme of dysmorphogenetic relatedness amongst different syndromes is illustrated.

Abnormalities, Multiple↗

PubMed1997

A member of the Met/HGF-receptor family is expressed in a BMP-4-like pattern in the ectoderm of Xenopus gastrulae.

The importance and involvement of growth factors and their corresponding receptors in embryonic induction has been more and more recognized during the past decade, in particular by loss-of-function experiments using dominant negative receptors. Here, we report the isolation of XHR, a Xenopus receptor-type tyrosine kinase, with homology to members of the Met/hepatocyte growth factor (HGF)-receptor family. Sequence comparison of XHR with other members of the Met/HGF-receptor family as well as in situ expression analyses suggest that XHR represents a novel member of this family of receptor-type tyrosine kinases. As could be shown by whole-mount in situ analysis, XHR transcripts are first expressed in the entire ectoderm at the onset of gastrulation. As gastrulation proceeds, XHR-transcription is turned off in cells induced by dorsal mesoderm to form neural tissue and thus, becomes predominantly confined to prospective epidermis. The strikingly similar expression patterns of XHR and Bone Morphogenetic Protein-4 (BMP-4), an inducer of epidermis and inhibitor of neural development, suggest an involvement of XHR signalling in the early cell-fate decision of ectodermal cells to form either neural derivatives or epidermis.

Animals↗

PubMed1998

A novel neuropeptide, Hym-176, induces contraction of the ectodermal muscle in Hydra.

During the course of a systematic non-targeting screening of peptide signal molecules in Hydra, we identified a novel myoactive neuropeptide called Hym-176. The primary structure of Hym-176 was determined to be APFIFPGPKVamide. It specifically and reversibly induced contraction of the ectodermal muscle of the hydra body column in vivo. However, it had no effect on the ectodermal muscle of the tentacles. The structure-activity relationship analysis showed that the sequence of FIFPGPKVamide is a minimal requirement for the myoactivity. Removal of an amide group from the C-terminus completely abolished the activity. By using the antibody specific to Hym-176, the tissue localization of the peptide in hydra was determined immunohistochemically. The intense immunoreactivity was found in the peduncle nerve cells, indicating that Hym-176 is a neuropeptide.

Amino Acid Sequence↗

PubMed2002

MSX2 expression in the apical ectoderm ridge is regulated by an MSX2 and Dlx5 binding site.

The apical ectodermal ridge (AER) is a specialized ectodermal region essential for limb outgrowth. Msx2 expression patterns in limb development strongly suggest an important role for Msx2 in the AER. Our previous studies identified a 348-bp fragment of the chicken Msx2 gene with AER enhancer activity. In this study, the functions of four potential homeodomain binding TAAT sites in this enhancer were studied using transgenic mice and in vitro protein-DNA interactions. Transgenic studies indicate that the four TAAT sites are not redundant and that only the B-TAAT site is critical for AER enhancer activity. The expression patterns of Msx2 and Dlx5 genes in the AER suggest that they might be involved in the regulation of Msx2. In support of this hypothesis, we found that Msx2 and Dlx5 can bind to the B-TAAT site as well as to a fragment containing the D- and E-TAAT sites in the Msx2 AER enhancer sequences. (c)2002 Elsevier Science (USA).

Animals↗

PubMed1993

The embryonic ciliated band of the sea urchin, Strongylocentrotus purpuratus derives from both oral and aboral ectoderm.

The ciliated band of the Strongylocentrotus purpuratus embryo consists of a columnar epithelium, 3-5 cells wide, which gives rise to a small number of neuroblasts. It arises late in development, as a border separating the squamous epithelial cells of the oral and aboral ectoderm. To determine the lineage origins of this structure, we performed double labeling experiments at the 2-cell stage and the 16-cell stage, which were designed to reveal clonal boundaries in the ciliated band. The ciliated band forms in a region of the ectoderm derived from descendants of the following blastomeres: No, VO, Na1u, Na2u, right and left NL1u, and right and left NL2u. In contrast to the lineage contributions of the embryonic territories established early in development, lineage origins of the ciliated band are variable. Specification of the ciliated band thus depends on intercellular interaction rather than lineage.

Animals↗

PubMed1997

XATH-1, a vertebrate homolog of Drosophila atonal, induces a neuronal differentiation within ectodermal progenitors.

XATH-1, a basic/helix-loop-helix transcription factor and a homolog of Drosophila atonal and mammalian MATH-1, is expressed specifically in the dorsal hindbrain during Xenopus neural development. In order to investigate the role of XATH-1 in the neuronal differentiation process, we have examined the effects of XATH-1 overexpression during Xenopus development. XATH-1 induces the expression of neuronal differentiation markers, such as N-tubulin, within the neural plate as well as within nonneural ectodermal progenitor populations, resulting in the appearance of process-bearing neurons within the epidermis. The related basic/helix-loop-helix genes neurogenin-related-1 and neuroD are not induced in response to XATH-1 overexpression within the embryo, suggesting that XATH-1 may activate an alternate pathway of neuronal differentiation. In further contrast to neurogenin-related-1 and neuroD, high-level expression of general neural markers expressed earlier in development, such as N-CAM, is not induced by XATH-1 overexpression. Competent ectodermal progenitors therefore respond to ectopic XATH-1 expression by initiating a distinct program of neuronal differentiation.

Amino Acid Sequence↗

PubMed1997

LiCl perturbs ectodermal veg1 lineage allocations in Strongylocentrotus purpuratus embryos.

In normal development the veg1 tier of the sixth cleavage Strongylocentrotus purpuratus embryo contributes progeny to both ectodermal lineages and portions of the archenteron. Treatment with 18 mM LiCl specifically affects this lineage allocation, reducing or eliminating the veg1 contribution to ectoderm. Less frequently this concentration of lithium causes the progeny of animal blastomeres to contribute to the archenteron.

Animals↗

PubMed1998

Defect in the maintenance of the apical ectodermal ridge in the Dactylaplasia mouse.

During vertebrate limb development the distal apex of the limb bud ectoderm is induced to form the apical ectodermal ridge (AER). The presence of the AER is required for the continued outgrowth of the limb bud. Classical embryological studies have led to the hypothesis that a secreted mesenchymal factor is required to maintain the AER. We have undertaken a detailed analysis of Dactylaplasia (Dac) mice, a semidominant mutant which displays missing central digits in the fore- and hindlimbs of heterozygous animals and monodactyly in homozygous animals. Our data show that Dac mice have a defect in the maintenance of the AER. At E10.5, the mutant AER is found to be morphologically normal. However, by E11.5 the central aspect of the AER degenerates leaving the anterior and posterior AER intact. In homozygous mice both the central and anterior AER degenerate, while the posterior extremity of the AER is unaffected. Analysis of BrdU incorporation reveals that degeneration of the AER is due to a lack of cell proliferation in the mutant AER. The loss of the AER leads to a reduction in cell proliferation in the subridge mesenchyme at E11.5. The data represent direct genetic evidence for the existence of an AER maintenance activity that is distinct from AER induction and differentiation. Moreover, the data suggest that the role of the AER maintenance factor is to promote cell proliferation in the ridge. Based on our findings, we propose a model for AER maintenance in the vertebrate limb.

Animals↗

PubMed1999

The neurotransmitter noradrenaline drives noggin-expressing ectoderm cells to activate N-tubulin and become neurons.

Neurotransmitters regulate neuronal function in the nervous system and modulation of their synthesis, release, and binding by immature neurons and their targets is a major part of nervous system development. We propose that the neurotransmitter noradrenaline regulates neuronal fate during neurulation, before neurons have differentiated. The ability of noradrenaline to induce a neural fate was tested in naive ectoderm caps cut from late blastula stage Xenopus embryos. Noradrenaline (10(-6) M) did not switch on otx-2 or NCAM and did not induce the formation of cement glands. We conclude that noradrenaline cannot induce a neural fate. By contrast, 10(-8) M noradrenaline activated N-tubulin in ectoderm caps expressing the neural inducing molecule noggin by the time intact siblings had become mid-neurulae. Methoxamine, a specific alpha-adrenergic receptor agonist, also activated N-tubulin in noggin-expressing caps. The alpha-adrenergic receptor blocker prazosin inhibited both noradrenaline- and methoxamine-induced activation of N-tubulin. The neurotransmitters dopamine and 5-HT did not activate expression of N-tubulin. XA-1, Otx-2, X-Delta, and Xotch transcripts were not sensitive to noradrenaline. HoxB9, which indicates posteriorization, was not activated by noradrenaline. When intact siblings were at stage 27, many cells in noggin-expressing, noradrenaline-treated caps were stained by the neuron-specific mcAb3A10. We propose that noradrenaline is an important endogenous modulator of neuronal fate, driving noggin-expressing cells to become neurons by binding to alpha-adrenergic receptors and activating a cascade that culminates in the expression of the neuronal markers N-tubulin and 3A10.

Animals↗