Relationship between the chemical structure of thiazolidine acetic acid derivatives and the antiherpetic activity in human embryonic cell cultures.
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Acetates↗
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Analysis of the structural integrity of YACs comprising human immunoglobulin genes in yeast and in embryonic stem cells.
With the goal of creating a strain of mice capable of producing human antibodies, we are cloning and reconstructing the human immunoglobulin germline repertoire in yeast artificial chromosomes (YACs). We describe the identification of YACs containing variable and constant region sequences from the human heavy chain (IgH) and kappa light chain (IgK) loci and the characterization of their integrity in yeast and in mouse embryonic stem (ES) cells. The IgH locus-derived YAC contains five variable (VH) genes, the major diversity (D) gene cluster, the joining (JH) genes, the intronic enhancer (EH), and the constant region genes, mu (C mu) and delta (C delta). Two IgK locus-derived YACs each contain three variable (V kappa) genes, the joining (J kappa) region, the intronic enhancer (E kappa), the constant gene (C kappa), and the kappa deleting element (kde). The IgH YAC was unstable in yeast, generating a variety of deletion derivatives, whereas both IgK YACs were stable. YACs encoding heavy chain and kappa light chain, retrofitted with the mammalian selectable marker, hypoxanthine phosphoribosyltransferase (HPRT), were each introduced into HPRT-deficient mouse ES cells. Analysis of YAC integrity in ES cell lines revealed that the majority of DNA inserts were integrated in substantially intact form.
Animals↗
Carbohydrate structure and cell differentitation: unique properties of fucosyl-glycopeptides isolated from embryonal carcinoma cells.
From embryonal carcinoma cells labeled with fucose, two main classes of glycopeptide products of Pronase digestion can be distinguished by Sephadex G-50 column chromatography: one eluted near the excluded volume and a smaller one. The large fucosyl-glycopeptides are scarcely present in differentiated cells derived from embryonal carcinoma cells (i.e., fibroblastlike cells, myoblasts, and parietal yolk-sac carcinoma). During in vitro differentiation of embryonal carcinoma cells, these large glycopeptides disappear almost completely. The small glycopeptides were analyzed by paper electrophoresis, concanavalin A-Sepharose affinity chromatography, and digestion with an endoglycosidase. The major components of these glycopeptides from embryonal carcinoma cells appear to be different from complex glycopeptides known to occur in adult cells. The glycopeptide pattern of mouse preimplantation embryos resembles that of embryonal carcinoma cells. These results suggest that the carbohydrate profile changes fundamentally during early stages of mammalian development.
Cell Differentiation↗
[Embryonal morphogenesis of the intraorgan circulatory bed, lymphatic outflow pathways and innervation structures].
Development of the circulation bed in human embryogenesis is brought about by a loop-like growth of vessels manifesting in proliferation, integration and morphofunctional transformation of the vascular loops. Proliferation of the loops ensures the blood inflow and reflux at all levels while their integration is followed by formation of hemocirculation system with appearance of the connective and major capillaries which serve the basis for development of true capillaries and capillary network in which precapillary arterioles and postcapillary venules can be distinguished. Hemocirculation system is completed by formation of the arteriolar and venular collaterals and arteriolo-venular anastomoses. Non-participation in the angiogenesis of the autogenic vessel endotheliocytes and their widespread necrosis give grounds to suggest that they are genetically condemned to death. Development of lymph vessels and innervation occurs simultaneously and together with blood vessels by mechanism of their centrifugal growth.
Cardiovascular System↗
[The pre- and postnatal development of the human lung].
The bronchoalveolar structures where studied during the intrauterine evolution by histological sections and pulmonary radiographs. This evolution depends on the degree of "prenatal immaturity" or "dismaturity". I compared my results with data from literature. I estimated the rate of bronchial growth as being not uniform, the most abundant branches being encountered in the basic layers of the inferior lobes, and some peripheral juxta-pleural bronchial bend in right angles, continuing with branches parallel to the pleural surface. I find justified the opinion, increasingly sustained by authors, that the epithelium of the bronchial conduction system has an endothelial origin, while the breathing device originates from the mesenchyme dressing the bronchial distal extremities. However, some pathological aspects, or pulmonary congenital abnormalities, make me sustain this double embryonal origin of the bronchoalveolar structures.
Bronchi↗
Lectin histochemistry of the embryonic heart: expression of terminal and penultimate galactose residues in developing rats and chicks.
Rat embryos at days 10-18 of gestation and chicken embryos at days 3-6 of incubation were fixed and processed for lectin histochemistry. The distribution of binding sites for a lectin from the peanut Arachis hypogaea (PNA) conjugated to horseradish peroxidase (HRP) was determined on tissue sections both before and after enzymatic cleavage of sialic acid with neuraminidase (sialidase). Endocardial cushion tissue in the rat, but not in the chick, reacted with PNA-HRP prior to digestion with sialidase. Endocardium of both species (12 and 13 days in rat, 5 and 6 days in chick), particularly at the level of endocardial cushions, reacted strongly with the sialidase-PNA sequence; this staining decreased markedly after day 14 of gestation in the rat. PNA binding sites capped by sialic acid were most abundant in the developing rat heart during the critical period of endocardial cushion formation and decreased as development proceeded. The marked changes in the appearance and distribution of cardiac cell and tissue glycoconjugates during cardiogenesis support the concept that rapid changes occur in the structure of complex carbohydrates during embryonic and fetal development. The findings also suggest that such glycosylation-related events may be species specific.
Animals↗
Effects of elevated cytoplasmic calcium and protein kinase C on endoplasmic reticulum structure and function in HEK293 cells.
In human embryonic kidney (HEK) cells stably transfected with green fluorescent protein targeted to the endoplasmic reticulum (ER), elevation of intracellular Ca2+ ([Ca2+]i) altered ER morphology, making it appear punctate. Electron microscopy revealed that these punctate structures represented circular and branched rearrangements of the endoplasmic reticulum, but did not involve obvious swelling or pathological fragmentation. Activation of protein kinase C with phorbol 12-myristate 13-acetate (PMA), prevented the effects of ionomycin on ER structure without affecting the elevation of [Ca2+]i. These results suggest that protein kinase C activation alters cytoplasmic or ER components underlying the effects of high [Ca2+]i on ER structure. Treatment of HEK cells with PMA also reduced the size of the thapsigargin-sensitive Ca2+ pool and inhibited Ca2+ entry in response to thapsigargin. Thus, protein kinase C activation has multiple actions on the calcium storage and signalling function of the endoplasmic reticulum in HEK cells: (1) reduced intracellular Ca2+ storage capacity, (2) inhibition of capacitative Ca2+ entry, and (3) protection of the endoplasmic reticulum against the effects of high [Ca2+]i.
Calcium↗
Computer-based three-dimensional visualization of developmental gene expression.
A broad understanding of the relationship between gene activation, pattern formation and morphogenesis will require adequate tools for three-dimensional and, perhaps four-dimensional, representation and analysis of molecular developmental processes. We present a novel, computer-based method for the 3D visualization of embryonic gene expression and morphological structures from serial sections. The information from these automatically aligned 3D reconstructions exceeds that from single-section and whole-mount visualizations of in situ hybridizations. In addition, these 3D models of gene-expression patterns can become a central component of a future developmental database designed for the collection and presentation of digitized, morphological and gene-expression data. This work is accompanied by a web site (http://www.univie.ac.at/GeneEMAC).
Anatomy, Cross-Sectional↗
Morphological and immunohistochemical characteristics of axial structures in the transitory human tail.
Ultrastructural relationships between the notochord and neighboring spinal cord were examined during the regression of the human tail. Also, the presence of certain extracellular matrix components in the notochord was immuno-histochemically analysed in the 4th to 12th week old embryos. At the early stages, a close apposition of the notochord to the spinal cord exists in the entire tail region. The external surface of both structures is covered with a continuous basal lamina. The narrow tissue interspace contains interdigitating cell processes and both amorphous and fibrillar extracellular matrix material. With advancing embryonic age, separation of the two structures occurs in craniocaudal direction and the widening interspace becomes occupied by mesenchymal cells. During tail regression and spinal cord retraction, the appearance of large intercellular spaces and cell degeneration takes place in both tissues. With age, the extracellular matrix of the notochord, predominantly the perinotochordal sheath, increases in amount and antigenic complexity. While the intensity of laminin, collagen type IV and type III expression rises continuously during the period examined, the expression of fibronectin begins first at later stages, after the separation of the notochord from the spinal cord. The possible developmental significance of the described phenomena in the regression of the posterior end of the human tail remains to be elucidated.
Animals↗
Concise review: epigenetic mechanisms contribute to pluripotency and cell lineage determination of embryonic stem cells.
Epigenetic mechanisms, such as histone modifications and DNA methylation, have been shown to play a key role in the regulation of gene transcription. Results of recent studies indicate that a novel "bivalent" chromatin structure marks key developmental genes in embryonic stem cells (ESCs), wherein a number of untranscribed lineage-control genes, such as Sox1, Nkx2-2, Msx1, Irx3, and Pax3, are epigenetically modified with a unique combination of activating and repressive histone modifications that prime them for potential activation (or repression) upon cell lineage induction and differentiation. However, results of these studies also showed that a subset of lineage-control genes, such as Myf5 and Mash1, were not marked by these histone modifications, suggesting that distinct epigenetic mechanisms might exist for lineage-control genes in ESCs. In this review article, we summarize evidence regarding possible mechanisms that control these unique histone modifications at lineage-control gene loci in ESCs and consider their possible contribution to ESC pluripotency. In addition, we propose a novel "histone modification pulsing" model wherein individual pluripotent stem cells within the inner cell mass of blastocysts undergo transient asynchronous histone modifications at these developmental gene loci, thereby conferring differential responsiveness to environmental cues and morphogenic gradients important for cell lineage determination. Finally, we consider how these rapid histone modification exchanges become progressively more stable as ESCs undergo differentiation and maturation into specialized cell lineages.
Animals↗
Synthesis, structural investigations on organotin(IV) chlorin-e6 complexes, their effect on sea urchin embryonic development and induced apoptosis.
Four new organotin(IV) chlorin derivatives, [chlorin=chlorin-e(6)=21H,23H-porphine-2-propanoic acid, 18-carboxy-20-(carboxymethyl)-8-ethenyl-13-ethyl-2,3-di-hydro-3,7,12,17-tetramethyl-(2S-trans)-], with formula (R(2)Sn)(3)(chlorin)(2).2H(2)O (R=Me, n-Bu) and (R(3)Sn)(3)chlorin.2H(2)O (R=Me, Ph) have been synthesized. The solid state and solution phase structures have been investigated by FT-IR, (119)Sn Mössbauer, (1)H and (13)C NMR spectroscopy. In the solid state, (R(2)Sn)(3)(chlorin)(2).2H(2)O complexes contain six coordinated Sn(IV), in a skew trapezoidal environment by forming trans-R(2)SnO(4) polymeric units. As far as (R(3)Sn)(3)chlorin.2H(2)O complexes are concerned, Sn(IV) is five coordinated in a polymeric (oligomeric) trigonal bipyramidal environment and eq-R(3)SnO(2) units, in the solid state. In saturated solutions, a polymeric structure comparable to the solid phase, with carboxylate groups of the ligand behaving in monoanionic bidentate fashion bridging Sn(IV) atoms, was detected for the (Me(3)Sn)(3)chlorin.2H(2)O complex, while in more diluted ones a tetrahedral configuration for the trimethyltin(IV) moieties was observed. Cytotoxic activity of the novel organotin(IV) chlorin was investigated in order to assay the effect on sea urchin embryonic development. The results obtained demonstrated that (n-Bu(2)Sn)(3)(chlorin)(2).2H(2)O and (Ph(3)Sn)(3)chlorin.2H(2)O exerted the antimitotic effect on the early stages of sea urchin development. In addition, the cytotoxic effect exerted by (n-Bu(2)Sn)(3)(chlorin)(2).2H(2)O appeared with necrosis of the blastomeres, which were clearly destroyed. After treatment with (Ph(3)Sn)(3)chlorin.2H(2)O, a programmed cell death was triggered, as shown by light microscope observations through morphological assays. The apoptotic events in 2-cell stage embryos revealed: (i) DNA fragmentation, with the TUNEL reaction (terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling); (ii) phosphatidylserine translocation in the membrane, with Annexin-V assay and (iii) cytoplasm blebbing, with the TUNEL reaction. The results demonstrated that the novel compound (Ph(3)Sn)(3)chlorin.2H(2)O was the most toxic derivative, by exerting antimitotic effect very early and by triggering apoptosis in the 2-cell stage of sea urchin embryonic development.
Animals↗
Accumulation of 210 kDa microtubule-interacting protein in differentiating P19 embryonal carcinoma cells.
The MA-01 antigen, a thermolabile 210 kDa microtubule-interacting protein, is present in P19 embryonal carcinoma cells on microtubular structures as well as in cytosol. After aggregation of the cells and subsequent incubation with all-trans-retinoic acid (RA), the level of MA-01 expression increased approximately 10 times during 15 days. The increase started after 2 days of incubation with RA and preceded the appearance of neuron-specific tubulin betaIII, MAP2C and neurofilaments. Such elevated expression of MA-01 antigen was not detected in P19 cells treated with dimethylsulfoxide. These data indicate that enhanced expression of MA-01 antigen is one of the earliest events occurring in P19 cells during neuronal differentiation.
Animals↗
The use of retinoids as probes for analyzing morphogenesis of glands from epithelial tissues.
Thirty-five years ago Honor Fell and Edward Mellanby were studying effects of high doses of vitamin A on skeletal development in chick embryos when they noticed that a piece of epidermis, accidentally included in an organ culture, had undergone mucous metaplasia. Further studies by Fell and others eventually led to an understanding of the important role of vitamin A in modulating epithelia in vivo. Fifteen years later another organ culture experiment showed me that excess vitamin A could also initiate the morphogenesis of branching and mucus-secreting glands from developing vibrissa follicles in upper lip skin of embryonic mice. Since then our group has shown that induction of this novel structure by naturally occurring retinoids resembles a normal embryonic induction in that it is stage-dependent, time-dependent, and irreversible. Tissue separation and recombination studies showed that isolated upper lip epidermis can form these glands when combined with retinoid-treated upper lip dermis. Untreated mouse epidermis can form similar glands after combination with chick dermis containing higher retinoid levels. The hamster cheek pouch, normally devoid of glandular structures, can also form mucous glands when treated with a retinoid, either in vivo or in vitro. Recombination studies in organ culture have now shown that mesenchyme exposed to retinoid is essential for gland morphogenesis from pouch epithelium. Evidence is accumulating that retinoic acid may even be the active morphogen in some normally developing systems.
Animals↗
Immunolocalization of latent transforming growth factor-beta binding protein-1 (LTBP1) during mouse development: possible roles in epithelial and mesenchymal cytodifferentiation.
Latent transforming growth factor-beta binding protein-1 (LTBP1) is a member of the fibrillin family; it is a glycoprotein of more than 190 kDa that is characterized by its possession of 16-18 epidermal growth factor-like motifs and 8 cysteine residues. The secretion of transforming growth factor-beta involves its release from cells in a large latent complex containing LTBP1, a latency-associated peptide, and the mature region of the growth factor. Using a polyclonal antibody specific for LTBP1 (Ab39), we examined the immunohistochemical localization of this molecule during mouse embryogenesis between 8.5 and 13.5 embryonic days. An extracellular fibrillar structure containing LTBP1 was found in both the basement membrane of epithelia and mesenchymal tissue in which extensive tissue remodeling is carried out. Immunoelectron microscopy revealed Ab39 immunoreactivity on a 5- to 10-nm microfibrillar component of these basement membranes as well as in mesenchymal tissue. These results suggest that LTBP1 is one of the extracellular microfibrillar components of the basement membrane and of mesenchymal tissue, and that it may play an important role in the regulation of developmental phenomena involved in epithelial-mesenchymal interaction and epithelial differentiation, processes in which transforming growth factor-beta is required for the control of cellular differentiation.
Animals↗
The spectrum of minimal clefting: process-oriented cleft management in the presence of an intact alveolus.
The minimal cleft lip provides a model for study of the clefting process. Nasolabial embryogenesis can be best understood using the concept of embryonic fields in which midline structures (columella, philtrum, premaxilla, septum, vomer, and ethmoids) develop with paired, fused A fields. Anatomic features of the minimal cleft lip suggest that the actual clefting site is located at the interface between the A and B fields within the lateral piriform wall. Study of the progression of clefting, using this model, places the timing of the clefting event to Carnegie stage 14. The degree to which this initial event affects subsequent fusion of the lateral and medial nasal processes (D and C fields) determines the final morphology of the cleft. Using this model, a rational basis is presented for the surgical management of minimal clefting in its varying manifestations.
Adult↗
Identification of novel chondroitin proteoglycans in Caenorhabditis elegans: embryonic cell division depends on CPG-1 and CPG-2.
Vertebrates produce multiple chondroitin sulfate proteoglycans that play important roles in development and tissue mechanics. In the nematode Caenorhabditis elegans, the chondroitin chains lack sulfate but nevertheless play essential roles in embryonic development and vulval morphogenesis. However, assignment of these functions to specific proteoglycans has been limited by the lack of identified core proteins. We used a combination of biochemical purification, Western blotting, and mass spectrometry to identify nine C. elegans chondroitin proteoglycan core proteins, none of which have homologues in vertebrates or other invertebrates such as Drosophila melanogaster or Hydra vulgaris. CPG-1/CEJ-1 and CPG-2 are expressed during embryonic development and bind chitin, suggesting a structural role in the egg. RNA interference (RNAi) depletion of individual CPGs had no effect on embryonic viability, but simultaneous depletion of CPG-1/CEJ-1 and CPG-2 resulted in multinucleated single-cell embryos. This embryonic lethality phenocopies RNAi depletion of the SQV-5 chondroitin synthase, suggesting that chondroitin chains on these two proteoglycans are required for cytokinesis.
Amino Acid Sequence↗
Depletion of three BMP antagonists from Spemann's organizer leads to a catastrophic loss of dorsal structures.
Transplanted Spemann's organizer induces dorsal embryonic cell fates such as the nervous system and somites, but in normal development, elimination of individual organizer signals (such as the bone morphogenetic protein [BMP] antagonists) has surprisingly modest effects on these tissues. Thus, the role of BMP antagonists may be limited to fine tuning the size of the dorsal domain. However, at least five BMP antagonists are specifically expressed in the organizer, and all can mimic aspects of organizer function, suggesting overlapping functions. Here, we deplete the function of three BMP antagonists, chordin, noggin, and follistatin, in Xenopus tropicalis. We demonstrate that this results in catastrophic failure of dorsal development and expansion of ventral and posterior fates. We conclude that BMP antagonists are required for formation of the neural plate and dorsal mesoderm. In addition, our results show that neural specification requires the continuous activity of BMP antagonists from blastula through gastrula stages.
Animals↗
Preserving the Pineal Gland in Perinatal Mouse Brain Preparations.
The pineal gland, a neuroendocrine structure that secretes melatonin, forms from an anlage at the dorsal midline in the embryonic forebrain. At embryonic day (E) 14.5 in the mouse, a pineal diverticulum is seen out-pouching from the roof of the diencephalon between the paired telencephalic vesicles. This diverticulum is in close contact with overlying cartilage, meningeal, and vascular tissue. It is easily lost when the cranial vault is opened to extract the brain at late embryonic/ early postnatal stages. Despite its important neuroendocrine role, the early development of the pineal gland and the signaling mechanisms that regulate this process remain poorly understood, partly due to the difficulty of preserving this structure intact during embryonic stages of mouse brain development. This article presents an innovative dissection procedure that preserves the pineal gland while maintaining its structural integrity and its attachment to the roof of the diencephalon during brain isolation from embryonic stages through postnatal day (P) 7. The procedure is demonstrated using an E18.5 mouse brain and is therefore suitable for downstream applications requiring preservation of tissue architecture, including in situ hybridization, immunohistochemistry, and spatial transcriptomics. The protocol may also be used to isolate the developing pineal gland, thereby improving pineal-specific representation in transcriptomic and proteomic analyses, which is otherwise challenging because of its small size.
Animals↗