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At least 973 records · Page 54Linked to original sources
PubMed2006

Impaired dendritic-cell function in ectodermal dysplasia with immune deficiency is linked to defective NEMO ubiquitination.

Ectodermal dysplasia with immune deficiency (EDI) is caused by alterations in NEMO (nuclear factor [NF]-kappaB essential modulator). Most genetic mutations are located in exon 10 and affect the C-terminal zinc finger domain. However, the biochemical mechanism by which they cause immune dysfunction remains undetermined. In this report, we investigated the effect of a cysteine-to-arginine mutation (C417R) found in the NEMO zinc finger domain on dendritic cell (DC) function. Following CD40 stimulation of DCs prepared from 2 unrelated patients with the NEMO C417R mutation, we found NEMO ubiquitination was absent, and this was associated with preserved RelA but absent c-Rel activity. As a consequence, CD40 stimulated EDI DCs failed to synthesize the c-Rel-dependent cytokine interleukin-12, had impaired up-regulation of costimulatory molecules, and failed to support allogeneic lymphocyte proliferation in vitro. In contrast, EDI DCs stimulated with the TLR4 ligand lipopolysaccharide (LPS) showed normal downstream NF-kappaB activity, DC maturation, and NEMO ubiquitination. These findings show for the first time how mutations in the zinc finger domain of NEMO can lead to pathway specific defects in NEMO ubiquitination and thus immune deficiency.

Arginine↗
PubMed2006

EDAR mutation in autosomal dominant hypohidrotic ectodermal dysplasia in two Swedish families.

BACKGROUND: Hypohidrotic ectodermal dysplasia (HED) is a genetic disorder characterized by defective development of teeth, hair, nails and eccrine sweat glands. Both autosomal dominant and autosomal recessive forms of HED have previously been linked to mutations in the ectodysplasin 1 anhidrotic receptor (EDAR) protein that plays an important role during embryogenesis. METHODS: The coding DNA sequence of the EDAR gene was analyzed in two large Swedish three-generational families with autosomal dominant HED. RESULTS: A non-sense C to T mutation in exon 12 was identified in both families. This disease-specific mutation changes an arginine amino acid in position 358 of the EDAR protein into a stop codon (p.Arg358X), thereby truncating the protein. In addition to the causative mutation two polymorphisms, not associated with the HED disorder, were also found in the EDAR gene. CONCLUSION: The finding of the p.Arg358X mutation in the Swedish families is the first corroboration of a previously described observation in an American family. Thus, our study strengthens the role of this particular mutation in the aetiology of autosomal dominant HED and confirms the importance of EDAR for the development of HED.

Abnormalities, Multiple↗
PubMed2003

Induction of cardiomyocytes by GATA4 in Xenopus ectodermal explants.

The earliest step in heart formation in vertebrates occurs during gastrulation, when cardiac tissue is specified. Dorsoanterior endoderm is thought to provide a signal that induces adjacent mesodermal cells to adopt a cardiac fate. However, the nature of this signalling and the precise role of endoderm are unknown because of the close proximity and interdependence of mesoderm and endoderm during gastrulation. To better define the molecular events that underlie cardiac induction, we have sought to develop a simple means of inducing cardiac tissue. We show that the transcription factor GATA4, which has been implicated in regulating cardiac gene expression, is sufficient to induce cardiac differentiation in Xenopus embryonic ectoderm (animal pole) explants, frequently resulting in beating tissue. Lineage labelling experiments demonstrate that GATA4 can trigger cardiac differentiation not only in cells in which it is present, but also in neighbouring cells. Surprisingly, cardiac differentiation can occur without any stable differentiation of anterior endoderm and is in fact enhanced under conditions in which endoderm formation is inhibited. Remarkably, cardiac tissue is formed even when GATA4 activity is delayed until long after explants have commenced differentiation into epidermal tissue. These findings provide a simple assay system for cardiac induction that may allow elucidation of pathways leading to cardiac differentiation. Better knowledge of the pathways governing this process may help develop procedures for efficient generation of cardiomyocytes from pluripotent stem cells.

Adaptor Proteins, Signal Transducing↗
PubMed2005

Loss of the extraembryonic ectoderm in Elf5 mutants leads to defects in embryonic patterning.

The extraembryonic ectoderm (ExE) is essential for mammalian placental formation and survival of the embryo in utero. We have obtained a mouse model lacking the ExE, by targeted deletion of the transcription factor Elf5. Although Elf5 mutant embryos implant and form an ectoplacental cone, no trophoblast stem (TS) cells can be derived, indicating that the absence of ExE is a result of the lack of TS cell maintenance. Embryos without ExE tissue are able to form the anterior visceral endoderm but fail to undergo gastrulation, demonstrating an essential role for the ExE in embryonic patterning during a defined window of development.

Animals↗
PubMed2005

Induction and migration of the anterior visceral endoderm is regulated by the extra-embryonic ectoderm.

The anterior visceral endoderm (AVE) is an extra-embryonic tissue required for specifying anterior pattern in the mouse embryo. The AVE is induced at the distal tip of the 5.5 dpc embryo and then migrates to the prospective anterior, where it imparts anterior identity upon the underlying epiblast (the tissue that gives rise to the embryo proper). Little is known about how the AVE is induced and what directs its migration. In this paper, we describe an essential role for another extra-embryonic tissue, the extra-embryonic ectoderm (ExE), in patterning the AVE and epiblast. Removal of the ExE in pre-gastrulation embryos leads to ectopic AVE formation, to a failure of AVE cell migration and to the assumption by the entire epiblast of an anterior identity. Ectopic transplantation of ExE cells inhibits AVE formation and leads to an expansion of the posterior epiblast marker T. These results demonstrate that the ExE restricts the induction of the AVE to the distal tip of the mouse embryo and is required to initiate the migration of these cells to the prospective anterior. Together, these data reveal a novel role for the ExE in the specification of the anteroposterior axis of the mouse embryo.

Animals↗
PubMed2006

Overexpression of NANOG in human ES cells enables feeder-free growth while inducing primitive ectoderm features.

Human embryonic stem cells (HESCs) are pluripotent cells derived from the ICM of blastocyst stage embryos. As the factors needed for their growth are largely undefined, they are propagated on feeder cells or with conditioned media from feeder cells. This is in contrast to mouse embryonic stem cells (MESCs) where addition of leukemia inhibitory factor (LIF) replaces the need for a feeder layer. Recently, the transcription factor Nanog was suggested to allow LIF and feeder-free growth of MESCs. Here, we show that NANOG overexpression in HESCs enables their propagation for multiple passages during which the cells remain pluripotent. NANOG overexpressing cells form colonies efficiently even at a very low density, an ability lost upon excision of the transgene. Cells overexpressing NANOG downregulate expression of markers specific to the ICM and acquire expression of a marker specific to the primitive ectoderm (the consecutive pluripotent population in the embryo). Examination of global transcriptional changes upon NANOG overexpression by DNA microarray analysis reveals new markers suggested to discriminate between these populations. These results are significant in the understanding of self-renewal and pluripotency pathways in HESCs, and of their use for modeling early development in humans.

Biomarkers↗
PubMed1987

Posterior apical ectodermal ridge removal in the chick wing bud triggers a series of events resulting in defective anterior pattern formation.

The ability of the anterior apical ectodermal ridge to promote outgrowth in the chick wing bud when disconnected from posterior apical ridge was examined by rotating the posterior portion of the stage-19/20 to stage-21 wing bud around its anteroposterior axis. This permitted contact between the anterior and posterior mesoderm, without removing wing bud tissue. In a small but significant number of cases (10/54), anterior structures (digit 2) formed spatially isolated from posterior structures (digits 3 and 4). Thus, continuity with posterior ridge is not a prerequisite for anterior-ridge function in the wing bud. Nevertheless, posterior-ridge removal does result in anterior limb truncation. To investigate events leading to anterior truncation, we examined cell death patterns in the wing bud following posterior-ridge removal. We observed an abnormal area of necrosis along the posterior border of the wing bud at 6-12 h following posterior-ridge removal. This was followed by necrosis in the distal, anterior mesoderm at 48 h postoperatively and subsequent anterior truncation. Clearly, healthy posterior limb bud mesoderm is needed for anterior limb bud survival and development. We propose that anterior truncation is the direct result of anterior mesodermal cell death and that this may not be related to positional specification of anterior cells. In our view, cell death of anterior mesoderm, after posterior mesoderm removal, should not be used as evidence for a role in position specification by the polarizing zone during the limb bud stages of development. We suggest that the posterior mesoderm that maintains the anterior mesoderm need not be restricted to the mapped polarizing zone, but is more extensively distributed in the limb bud.

Animals↗
PubMed1989

Expression of an engrailed-related protein is induced in the anterior neural ectoderm of early Xenopus embryos.

We have used a monoclonal antibody directed against the C-terminus of the Drosophila invected homeodomain to detect a nuclear protein in brain cells of Xenopus laevis embryos. We refer to this antigen as the Xenopus EN protein. The EN protein is localized at midneurula stage to a band of cells in the anterior portion of the neural plate, on each side of the neural groove. Later in development, the expression coincides with the boundary of the midbrain and hindbrain, and persists at least to the swimming tadpole stage. These properties make the EN protein an excellent molecular marker for anterior neural structures. In embryos where inductive interactions between mesodermal and ectodermal tissues have been perturbed, the expression of the EN protein is altered; in embryos that have been anterodorsalized by LiCl treatment, the region that expresses the EN protein is expanded, but still well organized. In ventralized UV-irradiated embryos, the absence of the protein is correlated with the absence of anterior neural structures. In extreme exogastrulae, where the contacts between head mesoderm and prospective neurectoderm are lost, the EN protein is not expressed.

Animals↗
PubMed1993

Mesoderm formation in Xenopus ectodermal explants overexpressing Xwnt8: evidence for a cooperating signal reaching the animal pole by gastrulation.

It is demonstrated here that the ability of injected Xwnt8 RNA to trigger mesoderm formation in Xenopus presumptive ectoderm (animal caps) depends on the time of explantation. Animal caps isolated from Xwnt8 injected embryos at the late blastula/early gastrula stages differentiate mesodermal tissues whereas caps isolated from early blastula do not. This finding suggests that an endogenous signal reaches the animal cap by the late blastula stage and cooperates with Xwnt8 to induce mesoderm. Similarly, late animal caps isolated at st. 10 from lithium-treated embryos, but not those from control embryos, elongate and express muscle-specific actin transcripts. In addition, the data presented suggests that the cooperating signal is distributed homogeneously with respect to the future dorsoventral axis and may require FGF- and activin-dependent signal transduction pathways. These observations support a model in which mesoderm is induced in vivo by a combined action of several different signals.

Animals↗
PubMed1994

Wingless can bring about a mesoderm-to-ectoderm induction in Drosophila embryos.

By means of nuclear transplantations, we make mosaics in which largely wingless- embryos contain patches of wingless+ cells. In these genetic mosaics, using a standard assay for wingless function (the maintenance of engrailed expression), we uncover an induction across germ layers: Wingless made in the mesoderm can sustain engrailed expression in the ectoderm. This result makes clear that Wingless is expressed in the mesoderm until at least one hour after gastrulation and may function in this germ layer in the wild type.

Animals↗
PubMed1996

The Caenorhabditis elegans LIN-26 protein is required to specify and/or maintain all non-neuronal ectodermal cell fates.

The C. elegans gene lin-26, which encodes a presumptive zinc-finger transcription factor, is required for hypodermal cells to acquire their proper fates. Here we show that lin-26 is expressed not only in all hypodermal cells but also in all glial-like cells. During asymmetric cell divisions that generate a neuronal cell and a non-neuronal cell, LIN-26 protein is symmetrically segregated and then lost from the neuronal cell. Expression in glial-like cells (socket and sheath cells) is biologically important, as some of these neuronal support cells die or seem sometimes to be transformed to neuron-like cells in embryos homozygous for strong loss-of-function mutations. In addition, most of these glial-like cells are structurally and functionally defective in animals carrying the weak loss-of-function mutation lin-26(n156). lin-26 mutant phenotypes and expression patterns together suggest that lin-26 is required to specify and/or maintain the fates not only of hypodermal cells but also of all other non-neuronal ectodermal cells in C. elegans. We speculate that lin-26 acts by repressing the expression of neuronal-specific genes in non-neuronal cells.

Animals↗
PubMed1998

XBF-1, a winged helix transcription factor with dual activity, has a role in positioning neurogenesis in Xenopus competent ectoderm.

Neuronal differentiation in the vertebrate nervous system is temporally and spatially controlled by mechanisms which are largely unknown. Here we investigate the role of XBF-1, an anterior neural plate-specific winged helix transcription factor, in controlling the pattern of neurogenesis in Xenopus ectoderm. We show that, in the anterior neural plate of normal embryos, prospective neurogenesis is positioned at the anterior boundary of the XBF-1 expression domain. By misexpressing XBF-1 in the posterior neural plate we show that a high dose of XBF-1 has a dual effect; it suppresses endogenous neuronal differentiation in high expressing cells and induces ectopic neuronal differentiation in adjacent cells. In contrast, a low dose of XBF-1 does not suppress but instead, expands the domain of neuronal differentiation in the lateral and ventral sides of the embryo. XBF-1 regulates the expression of XSox3, X-ngnr-1, X-Myt-1 and X-&Dgr;-1 suggesting that it acts early in the cascade leading to neuronal differentiation. A fusion of XBF-1 to a strong repressor domain (EnR) mimics most of the XBF-1 effects suggesting that the wild type XBF-1 is a transcriptional repressor. However, fusion of XBF-1 to a strong activation domain (E1A) specifically suppresses neuronal differentiation suggesting that XBF-1 may also work as a transcriptional activator. Based on these findings, we propose that XBF-1 is involved in positioning neuronal differentiation by virtue of its concentration dependent, dual activity, as a suppressor and an activator of neurogenesis.

Amino Acid Sequence↗
PubMed2000

Region-specific activation of the Xenopus brachyury promoter involves active repression in ectoderm and endoderm: a study using transgenic frog embryos.

Tissue specification in the early embryo requires the integration of spatial information at the promoters of developmentally important genes. Although several response elements for signalling pathways have been identified in Xenopus promoters, it is not yet understood what defines the sharp borders that restrict expression to a specific tissue. Here we use transgenic frog embryos to study the spatial and temporal regulation of the Xbra promoter. Deletion analysis and point mutations in putative transcription factor-binding sites identified two repressor modules, which exert their main effects at different stages during gastrulation. One module is defined by a bipartite binding site for a Smad-interacting protein (SIP1) of the deltaEF1 repressor family and acts to confine expression to the marginal zone early in gastrulation. The other module is defined by two homeodomain-binding sites and is responsible for repression in dorsal mesoderm and ectoderm at mid-gastrula stages. In addition, an upstream region of the promoter is necessary to repress expression in neural tissues later in development. Together, our results show that repression plays an important role in the restriction of Xbra expression to the mesoderm, and we suggest that similar mechanisms may be involved in the spatial regulation of other genes in early embryonic development.

Animals↗
PubMed1983

Conditioning of a culture substratum by the ectodermal layer promotes attachment and oriented locomotion by amphibian gastrula mesodermal cells.

We have found that ectodermal fragments of Ambystoma maculatum gastrulae deposit immense numbers of 0.1 micron diameter extracellular fibrils on plastic coverslips. When migrating mesodermal cells from A. maculatum gastrulae are seeded on such conditioned plastic substrata, they attach and begin migrating after 15-30 min in vitro. We did a detailed analysis of the relationship between fibril orientation and cell migration using time-lapse cinemicrography, scanning electron microscopy, and a microcomputer with a graphics tablet and morphometric program. We found that cells move in directions closely related to the orientation of fibrils. Usually fibrils are oriented in dense arrays with a predominance of fibrils running parallel to the blastopore-animal pole axis of the explant, and cells move preferentially along lines parallel to the blastopore-animal pole axis. When fibrils are unaligned, cells move at random. We have also shown that cells move with a slightly stronger tendency towards the animal pole direction. These results are discussed concerning the mechanism of specific cell migration during amphibian gastrulation.

Ambystoma↗
PubMed1983

Comparative study of extracellular fibrils on the ectodermal layer in gastrulae of five amphibian species.

Previous studies have shown the presence of a network of extracellular fibrils on the inner surface of the ectodermal layer of the Ambystoma maculatum gastrulae. The alignment of the network along the blastopore-animal pole axis has suggested that the network of fibrils guides the migrating mesodermal cells in gastrulae by contact guidance. We have also shown that these fibrils can be deposited on substrata by explanted embryonic fragments and that substrata conditioned in this manner support directed cell migration. In this study, we found that the appearance of the fibrils in the embryos coincides with the start of cell migration towards the animal pole. Gastrulae of three urodele species examined (A. maculatum, A. mexicanum and Cynops pyrrhogaster) have similar dense networks of fibrils. Xenopus laevis gastrulae also have similar fibrils but fewer fibrils compared to urodele embryos. Rana pipiens gastrulae have very few extracellular fibrils. The scarcity of the fibrils in anuran species may be related to the differences in arrangement of mesodermal cells during migration.

Ambystoma↗
PubMed1975

The transmission of impulses in the ectodermal slow conduction system of the sea anemone Calliactis parasitica (Couch).

1. The SS 1 fatigues in response to repetitive electrical stimulation. This fatigue is manifested by an increased conduction delay and a decreased SS 1 pulse amplitude. 2. Continued repetitive stimulation leads to the failure of the system. Recovery may take many seconds. Narrow strips of column fail more rapidly than wide strips. 3. The increased conduction delay is explained in terms of a decrease in the population of spiking cells. 4. A computer model is described and analysed. It suggests that conduction between electrically coupled ectoderm cells could be the basis for the SS1. The SS 1 may have properties not so far experimentally demonstrated; for example, under certain conditions it could behave as a local system.

Animals↗
PubMed2004

Anhidrotic ectodermal dysplasia presenting as atrophic rhinitis.

Atrophic rhinitis is a chronic inflammatory disease of the nose. The aetiology of primary atrophic rhinitis is not yet known, although secondary atrophic rhinitis is known to be associated with chronic granulomatous diseases such as tuberculosis and leprosy. The authors report a case of atrophic rhinitis, which was a presenting feature of a rare genetic disorder known as Christ-Siemens-Touraine syndrome, also known as anhidrotic ectodermal dysplasia.

Adult↗