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PubMed1991

Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins: intermediate generalizations.

A previous rendition of a mechanism for the induction of embryonic gene activity, derived from the viewpoint of agents capable of such inductions, concluded that a perturbed methylation pattern of DNA and/or chromatin proteins would be an essential feature. A more specific treatment of the mechanism centers on enhancer regions of proto-oncogenes as being the point of modification for any induction of new gene activity. DNA binding type proteins may be involved with deheterochromatization processes after complexing near long terminal repeat segments containing enhancer elements. Chemical carcinogens and steroids would modify the chromatin and directly or indirectly interfere with maintenance DNA methylation. The resulting hypomethylated enhancer and promoter regions would allow for enhancer mechanisms to activate repressed embryonic genes inappropriate to the developmental stage forcing embryonic features to be expressed by differentiating (or differentiated) cells.

Animals↗
PubMed2001

HMG-17 is an early marker of inductive interactions in the developing mouse kidney.

We studied the relationship between proliferation, differentiation, and the expression of high-mobility-group protein 17 (HMG-17) during metanephric kidney development. Proliferating cells were found homogenously throughout the early kidney rudiment. The expression pattern of HMG-17 mRNA, on the other hand, was distinctly uneven: In the undifferentiated mesenchyme, the cells in the cranial "tail" part of the mesenchyme showed only a weak signal, whereas a group of cells lying close to the tip of the ureteric bud showed strong HMG-17 expression. The region distinctly positive for HMG-17 is known to contain the first cells to undergo mesenchyme-to-epithelium transition. Using the transfilter model system, strong expression of HMG-17 mRNA, followed by mesenchyme-to-epithelium transition, could be induced also in the "tail" part of the mesenchyme. The upregulation of HMG-17 in the metanephrogenic mesenchyme thus results from interaction with an inductor tissue. Throughout the renal development, the HMG-17 mRNA was also abundant in those epithelial and mesenchymal cells that were undergoing active cell differentiation, and the transcript was downregulated in mature cells. HMG-17 expression thus correlated with the processes of induction and differentiation rather than with proliferation. The present results suggest that HMG-17 could have a role in the activation of the genes regulating kidney organogenesis.

Animals↗
PubMed2003

Prox1, master regulator of the lymphatic vasculature phenotype.

In contrast to the extensive molecular and functional characterization of blood vascular endothelium, little is known about the mechanisms that control the formation and lineage-specific differentiation and function of lymphatic vessels. The homeobox gene Prox1, the vertebrate homologue of the Drosophila prospero gene, has been recently identified to be required for the induction of lymphatic vascular development from preexisting embryonic veins, and studies in Prox1-deficient mice have confirmed Florence Sabin's original hypothesis about the origin of the lymphatic vascular system from embryonic veins. The recent establishment of cell culture models for the selective propagation of blood vascular and lymphatic endothelial cells, together with the findings that these cells maintain their lineage-specific differentiation in vitro, has led to the discovery that Prox1 expression is sufficient to induce a lymphatic phenotype in blood vascular endothelium. Ectopic expression of Prox1 downregulated blood vascular-associated genes and also upregulated some of the known lymphatic endothelial cell markers. Together, these studies suggest that the blood vascular phenotype represents the default endothelial differentiation and they identify an essential role of Prox1 in the program specifying lymphatic endothelial cell fate.

Amino Acid Sequence↗
PubMed1996

How is myogenesis initiated in the embryo?

Skeletal myoblasts are derived from paraxial mesoderm, but how myoblasts acquire their identity is still a matter of speculation. The characterization of molecular markers and, in some cases, the analysis of mutations in the corresponding genes, has now made it possible to ask specific questions about this process. Specification of somite cell fate depends on epigenetic factors. Adjacent tissues, such as the neural tube, notochord, dorsal ectoderm and lateral mesoderm, act either positively or negatively on the different myogenic precursor populations in the somite. Candidate molecules for this complex signalling activity include sonic hedgehog and the Wnt proteins as positive signals, and BMP4 as a possible inhibitor. Although it is generally assumed that induction is required, some observations suggest that embryonic cells might have a tendency to undergo myogenesis as a 'default' pathway. By analogy with Drosophila, where the neurogenic genes affect myogenesis, the vertebrate homologues of notch and its ligands could be candidate molecules for a repression or derepression mechanism. Similar studies with cultured muscle cells also implicate other HLH factors as potential inhibitors of the MyoD family and, hence, of inappropriate myogenesis.

Animals↗
PubMed1979

Induction of glutamine synthetase in embryonic neural retina: localization in Müller fibers and dependence on cell interactions.

The cellular localization of glutamine synthetase [GSase; L-glutamate:ammonia ligase(ADP)-forming), EC 6.3.1.2] induced by cortisol in the neural retina of chicken embryos was investigated by immunostaining with GSase-specific antiserum and indirect immunofluorescence. In organ cultures of retina tissue, and in the retina in vivo, hormone-induced GSase was found to be confined only to the Müller fibers (retinoglia). Also, in mature chicken retina, which contains a very high level of GSase, the enzyme was detected solely in Müller fibers. In short-term monolayer cultures of dispersed embryonic retina cells, there was no GSase induction and no immunodetectable increase in enzyme level. However, when the dispersed cells were reaggregated and they restituted retinotypic cell associations, GSase could be induced and it was localized in Müller fibers. The results suggest that, in addition to the hormonal stimulus, contact-dependent interactions between Müller glia cells and retina neurons are involved in the mechanism of GSase induction in the retina.

Animals↗
PubMed2004

brinker and optomotor-blind act coordinately to initiate development of the L5 wing vein primordium in Drosophila.

The stereotyped pattern of Drosophila wing veins is determined by the action of two morphogens, Hedgehog (Hh) and Decapentaplegic (Dpp), which act sequentially to organize growth and patterning along the anterior-posterior axis of the wing primordium. An important unresolved question is how positional information established by these morphogen gradients is translated into localized development of morphological structures such as wing veins in precise locations. In the current study, we examine the mechanism by which two broadly expressed Dpp signaling target genes, optomotor-blind (omb) and brinker (brk), collaborate to initiate formation of the fifth longitudinal (L5) wing vein. omb is broadly expressed at the center of the wing disc in a pattern complementary to that of brk, which is expressed in the lateral regions of the disc and represses omb expression. We show that a border between omb and brk expression domains is necessary and sufficient for inducing L5 development in the posterior regions. Mosaic analysis indicates that brk-expressing cells produce a short-range signal that can induce vein formation in adjacent omb-expressing cells. This induction of the L5 primordium is mediated by abrupt, which is expressed in a narrow stripe of cells along the brk/omb border and plays a key role in organizing gene expression in the L5 primordium. Similarly, in the anterior region of the wing, brk helps define the position of the L2 vein in combination with another Dpp target gene, spalt. The similar mechanisms responsible for the induction of L5 and L2 development reveal how boundaries set by dosage-sensitive responses to a long-range morphogen specify distinct vein fates at precise locations.

Animals↗
PubMed1992

Expression cloning of noggin, a new dorsalizing factor localized to the Spemann organizer in Xenopus embryos.

We have cloned a cDNA encoding a novel polypeptide capable of inducing dorsal development in Xenopus embryos. RNA transcripts from this clone rescue normal development when injected into ventralized embryos and result in excessive head development at high doses. Therefore, we have named the cDNA noggin, noggin cDNA contains a single reading frame encoding a 26 kd protein with a hydrophobic amino-terminal sequence, suggesting that it is secreted. In Northern blot analysis this cDNA hybridizes to two mRNAs that are expressed both maternally and zygotically. Although noggin transcript is not localized in the oocyte and cleavage stage embryo, zygotic transcripts are initially restricted to the presumptive dorsal mesoderm and reach their highest levels at the gastrula stage in the dorsal lip of the blastopore (Spemann organizer). In the neurula, noggin is transcribed in the notochord and prechordal mesoderm. The activity of exogenous noggin RNA in embryonic axis induction and the localized expression of endogenous noggin transcripts suggest that noggin plays a role in normal dorsal development.

Amino Acid Sequence↗
PubMed1995

Induction of a secondary embryonic axis in zebrafish occurs following the overexpression of beta-catenin.

Formation of the vertebrate axis may involve a Wnt signaling cascade similar to the Drosophila wingless pathway. Zebrafish wnt8 is a candidate for involvement in axis specification insofar as it is expressed maternally and when overexpressed it can induce goosecoid, a transcription factor normally expressed in the embryonic shield. In this study we demonstrate that beta-catenin, a cadherin associated protein in the Wnt pathway, is expressed maternally in zebrafish and is widely distributed in the early embryo. Overexpressing beta-catenin in early zebrafish embryos induces goosecoid and ntl, ultimately leading to a duplication of a complete secondary axis. These data are consistent with the involvement of beta-catenin in a Wnt signaling pathway which is involved in mesoderm induction in zebrafish.

Amino Acid Sequence↗
PubMed2000

The morphogenetic role of midline mesendoderm and ectoderm in the development of the forebrain and the midbrain of the mouse embryo.

The anterior midline tissue (AML) of the late gastrula mouse embryo comprises the axial mesendoderm and the ventral neuroectoderm of the prospective forebrain, midbrain and rostral hindbrain. In this study, we have investigated the morphogenetic role of defined segments of the AML by testing their inductive and patterning activity and by assessing the impact of their ablation on the patterning of the neural tube at the early-somite-stage. Both rostral and caudal segments of the AML were found to induce neural gene activity in the host tissue; however, the de novo gene activity did not show any regional characteristic that might be correlated with the segmental origin of the AML. Removal of the rostral AML that contains the prechordal plate resulted in a truncation of the head accompanied by the loss of several forebrain markers. However, the remaining tissues reconstituted Gsc and Shh activity and expressed the ventral forebrain marker Nkx2.1. Furthermore, analysis of Gsc-deficient embryos reveals that the morphogenetic function of the rostral AML requires Gsc activity. Removal of the caudal AML led to a complete loss of midline molecular markers anterior to the 4th somite. In addition, Nkx2.1 expression was not detected in the ventral neural tube. The maintenance and function of the rostral AML therefore require inductive signals emanating from the caudal AML. Our results point to a role for AML in the refinement of the anteroposterior patterning and morphogenesis of the brain.

Animals↗
PubMed2001

LDL-receptor-related protein 6 is a receptor for Dickkopf proteins.

Wnt glycoproteins have been implicated in diverse processes during embryonic patterning in metazoa. They signal through frizzled-type seven-transmembrane-domain receptors to stabilize beta-catenin. Wnt signalling is antagonized by the extracellular Wnt inhibitor dickkopf1 (dkk1), which is a member of a multigene family. dkk1 was initially identified as a head inducer in Xenopus embryos but the mechanism by which it blocks Wnt signalling is unknown. LDL-receptor-related protein 6 (LRP6) is required during Wnt/beta-catenin signalling in Drosophila, Xenopus and mouse, possibly acting as a co-receptor for Wnt. Here we show that LRP6 (ref. 7) is a specific, high-affinity receptor for Dkk1 and Dkk2. Dkk1 blocks LRP6-mediated Wnt/beta-catenin signalling by interacting with domains that are distinct from those required for Wnt/Frizzled interaction. dkk1 and LRP6 interact antagonistically during embryonic head induction in Xenopus where LRP6 promotes the posteriorizing role of Wnt/beta-catenin signalling. Thus, DKKs inhibit Wnt co-receptor function, exemplifying the modulation of LRP signalling by antagonists.

Adaptor Proteins, Signal Transducing↗
PubMed1981

Induction of glutamine synthetase in embryonic neural retina: its suppression by the gliatoxic agent alpha-aminoadipic acid.

Competence for cortisol-mediated induction of glutamine synthetase (GS) is a differentiation marker of embryonic neural retina. Earlier work has indicated that the induction and accumulation of GS is localized in the Müller glia cells. This localization was presently confirmed by the finding that the gliatoxin D,L-alpha-amino-adipic acid (AAA) reduces responsiveness to GS induction by 60--90% due to preferential damage to Müller cells. The tests were performed on organ cultures of retina tissue from chick embryos, and on retina cell aggregates in which there is tissue reconstruction. The presence of GS-inducible Müller cells was monitored by immuno-staining of tissue sections with anti-GS antiserum. Reduction of GS inducibility due to pretreatment with AAA resulted in virtual absence of cells that immunostained for GS. The preferential toxicity of AAA for Müller cells was also demonstrated by cell viability tests; it was further corroborated by the finding that treatment with AAA greatly reduced the level of carbonic anhydrase activity, another enzyme localized predominantly in Müller cells, but did not affect gamma-aminobutyric acid transaminase and choline acetyl transferase, neuronal enzymes. Susceptibility of Müller cells to AAA was found to increase with embryonic development of the retina. We suggest that acquisition of susceptibility for AAA represents another differentiation marker of embryonic Müller cells.

2-Aminoadipic Acid↗
PubMed2007

In vitro gamete derivation from pluripotent stem cells: progress and perspective.

Germ cells constitute a highly specialized cell population that is indispensable for the continuation and evolution of the species. Recently, several research groups have shown that these unique cells can be produced in vitro from pluripotent stem cells. Furthermore, live births of offspring using induced germ cells have been reported in one study. These results suggest that it may be possible to investigate germ cell development ex vivo and to establish novel reproductive technologies. To this end, it is critical to assess if gamete induction processes in vitro faithfully recapitulate normal germ cell development in vivo. Here, this issue is discussed with a focus on the germ line specification and the sex-specific development of pre- and postnatal germ cells. The aim of this paper is to concisely summarize the past progress and to present some future issues for the investigation into in vitro gamete production from pluripotent stem cells.

Animals↗
PubMed1998

Developmental expression patterns of mouse sFRP genes encoding members of the secreted frizzled related protein family.

Development of the metanephric kidney is an experimental model system to analyze interactions between mesenchymal and epithelial cells and mesenchymal-epithelial transition. To study the underlying genetic mechanisms we employed organ culture and differential display PCR to identify genes regulated upon induction of mesenchymal cells. One of the genes found encodes the secreted frizzled related protein 2 (sFRP2) that is upregulated within 2 days of in vitro development. In vivo sFRP2 expression was likewise found in mesenchymal condensates and subsequent epithelial structures. Detailed in situ hybridization analysis revealed sFRP2 expression during development of the eye, brain, neural tube, craniofacial mesenchyme, joints, testis, pancreas and below the epithelia of oesophagus, aorta and ureter where smooth muscles develop. In a comparative analysis transcripts of the related sFRP1 and sFRP4 genes were frequently found in the same tissues as sFRP2 with their expression domains overlapping in some instances, but mutually exclusive in others. While sFRP1 is specifically expressed in the embryonic metanephros, eye, brain, teeth, salivary gland and small intestine, there is only weak expression of sFRP4 except for the developing teeth, eye and salivary gland. The interpretation of the highly specific spatial and temporal expression patterns of sFRP genes will partly depend on a better functional understanding of the interaction between wnt, fz and sFRP family members. Nevertheless, sFRP genes must play quite distinct roles in the morphogenesis of several organ systems.

Animals↗
PubMed2006

One-step induction of neurons from mouse embryonic stem cells in serum-free media containing vitamin B12 and heparin.

We present a simple method for neural cell fate specification directly from mouse embryonic stem cells (ES cells) in serum-free conditions in the absence of embryoid body formation. Dissociated ES cells were cultured in serum-free media supplemented with vitamin B12 and heparin, but without any expensive cytokines. After 14 days in culture, beta-tubulin type III (TuJ1) and tyrosine hydroxylase (TH)-positive colonies were detected by immunocytochemical examinations. In addition, specific gene analyses by RT-PCR demonstrated expression of an early central nerve system, mature neuron, and midbrain dopaminergic neuron-specific molecules (i.e., nestin, middle molecular mass neurofilament protein, Nurr1, and TH, respectively). Dopamine was also detected in the culture media by reverse-phase HPLC analysis. These facts indicate that addition of vitamin B12/heparin to serum-free culture media induced neurons from ES cells, which included cells that released dopamine. Other supplements, such as putrescine, biotin, and Fe2+, could not induce neurons from ES cells by themselves, but produced synergistic effects with vitamin B12/heparin. The rate of TuJ1+/TH+ colony formation was increased threefold and the amounts of dopamine released increased 1.5-fold by the addition of a mixture of putrescine, biotin, and Fe2+ to vitamin B12/heparin culture media. Our method is a simple tool to differentiate ES cells to dopaminergic neurons for the preparation of dopamine-releasing cells for the cell transplantation therapy of Parkinson's disease. In addition, this method can facilitate the discovery of soluble factors and genes that can aid in the induction of the ES cell to its neural fate.

Animals↗
PubMed2003

Msx homeobox gene family and craniofacial development.

Vertebrate Msx genes are unlinked, homeobox-containing genes that bear homology to the Drosophila muscle segment homeobox gene. These genes are expressed at multiple sites of tissue-tissue interactions during vertebrate embryonic development. Inductive interactions mediated by the Msx genes are essential for normal craniofacial, limb and ectodermal organ morphogenesis, and are also essential to survival in mice, as manifested by the phenotypic abnormalities shown in knockout mice and in humans. This review summarizes studies on the expression, regulation, and functional analysis of Msx genes that bear relevance to craniofacial development in humans and mice. Key words: Msx genes, craniofacial, tooth, cleft palate, suture, development, transcription factor, signaling molecule.

Animals↗
PubMed1998

Formation of Rathke's pouch requires dual induction from the diencephalon.

Targeted disruption of the homeobox gene T/ebp (Nkx2.1, Ttf1, Titf1) in mice results in ablation of the pituitary. Paradoxically, while T/ebp is expressed in the ventral diencephalon during forebrain formation, it is not expressed in Rathke's pouch or in the pituitary gland at any time of embryogenesis. Examination of pituitary development in the T/ebp homozygous null mutant embryos revealed that a pouch rudiment is initially formed but is eliminated by programmed cell death before formation of a definitive pouch. In the diencephalon of the mutant, Bmp4 expression is maintained, whereas Fgf8 expression is not detectable. These data and additional genetic and molecular observations suggest that Rathke's pouch develops in a two-step process that requires at least two sequential inductive signals from the diencephalon. First, BMP4 is required for induction and formation of the pouch rudiment, a role confirmed by analysis of Bmp4 homozygous null mutant embryos. Second, FGF8 is necessary for activation of the key regulatory gene Lhx3 and subsequent development of the pouch rudiment into a definitive pouch. This study provides firm molecular genetic evidence that morphogenesis of the pituitary primordium is induced in vivo by signals from the adjacent diencephalon.

Animals↗
PubMed2005

Collection of neural inducing factors from PA6 cells using heparin solution and their immobilization on plastic culture dishes for the induction of neurons from embryonic stem cells.

Embryonic stem (ES) cells have the ability to replicate themselves and differentiate into various mature cells. Recently, dopaminergic neurons were efficiently induced from ES cells using mouse stromal cells (PA6 cells) as a feeder cell layer. This simple procedure seems to be very efficient to obtain dopamine-releasing cells for future clinical cell transplantation treatment of Parkinson's disease. In this study, we prepared stock solutions containing neural inducing factors (NIFs) by washing PA6 cells with phosphate-buffered saline containing heparin. ES cells grew successfully in culture media supplemented with 33 v/v% NIFs stock solution, and the rate of neural differentiation of ES cell progeny increased with increasing heparin concentration in the culture media. In addition, NIFs-immobilized surfaces were prepared by exposing polyethyleneimine-modified surfaces to NIFs stock solutions. The NIFs-immobilized culture dish effectively supported cell growth as the culture medium supplemented with NIFs stock did, but its induction effect to dopaminergic neurons from ES cells was much smaller than free NIFs. NIFs stock solutions have two different activities. One can stimulate cell growth and the other induces differentiation of ES cells to the neural fate when heparin existed. The former factors were effectively immobilized on the culture dish, but those that induce differentiation may not be. Further optimization is required.

Animals↗