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PubMed1999

Expression and functional analysis of Cititf1, an ascidian NK-2 class gene, suggest its role in endoderm development.

In solitary ascidians the fate of endoderm is determined at a very early stage of development and depends on cytoplasmic factors whose nature has not been determined. We have isolated a member of the NK-2 gene family, Cititf1, from the ascidian Ciona intestinalis, showing high sequence homology to mammalian TITF1. The Cititf1 gene was expressed in all endodermal precursors at the pregastrula and gastrula stages, and is thus the first specific regulatory endodermal marker to be isolated from an ascidian. Cititf1 expression was downregulated at the end of gastrulation to reappear at middle tailbud and larval stages in the most anterior and ventral parts of head endoderm, regions which give rise, after metamorphosis, to the adult endostyle, where Cititf1 mRNA was still present. Microinjection of Cititf1 mRNA into fertilized eggs resulted in tadpole larvae with abnormalities in head-trunk development consequent to the formation of excess endoderm, perhaps due to recruitment of notochord precursors to an endodermal fate. These data suggest that Cititf1 plays an important role in normal endoderm differentiation during ascidian embryogenesis.

Animals↗
PubMed2000

(beta)-catenin mediates the specification of endoderm cells in ascidian embryos.

In the present study, we addressed the role of (beta)-catenin in the specification of embryonic cells of the ascidians Ciona intestinalis and C. savignyi and obtained the following results: (1) During cleavages, (beta)-catenin accumulated in the nuclei of vegetal blastomeres, suggesting that it plays a role in the specification of endoderm. (2) Mis- and/or overexpression of (beta)-catenin induced the development of an endoderm-specific alkaline phosphatase (AP) in presumptive notochord cells and epidermis cells without affecting differentiation of primary lineage muscle cells. (3) Downregulation of (beta)-catenin induced by the overexpression of cadherin resulted in the suppression of endoderm cell differentiation. This suppression was compensated for by the differentiation of extra epidermis cells. (4) Specification of notochord cells did not take place in the absence of endoderm differentiation. Both the overexpression of (beta)-catenin in presumptive notochord cells and the downregulation of (beta)-catenin in presumptive endoderm cells led to the suppression of Brachyury gene expression, resulting in the failure of notochord specification. These results suggest that the accumulation of (beta)-catenin in the nuclei of endoderm progenitor cells is the first step in the process of ascidian endoderm specification.

Alkaline Phosphatase↗
PubMed2000

The concentric structure of the developing gut is regulated by Sonic hedgehog derived from endodermal epithelium.

The embryonic gut of vertebrates consists of endodermal epithelium, surrounding mesenchyme derived from splanchnic mesoderm and enteric neuronal components derived from neural crest cells. During gut organogenesis, the mesenchyme differentiates into distinct concentric layers around the endodermal epithelium forming the lamina propria, muscularis mucosae, submucosa and lamina muscularis (the smooth muscle layer). The smooth muscle layer and enteric plexus are formed at the outermost part of the gut, always some distance away from the epithelium. How this topographical organization of gut mesenchyme is established is largely unknown. Here we show the following: (1) Endodermal epithelium inhibits differentiation of smooth muscle and enteric neurons in adjacent mesenchyme. (2) Endodermal epithelium activates expression of patched and BMP4 in adjacent non-smooth muscle mesenchyme, which later differentiates into the lamina propria and submucosa. (3) Sonic hedgehog (Shh) is expressed in endodermal epithelium and disruption of Shh-signaling by cyclopamine induces differentiation of smooth muscle and a large number of neurons even in the area adjacent to epithelium. (4) Shh can mimic the effect of endodermal epithelium on the concentric stratification of the gut. Taken together, these data suggest that endoderm-derived Shh is responsible for the patterning across the radial axis of the gut through induction of inner components and inhibition of outer components, such as smooth muscle and enteric neurons.

Animals↗
PubMed2001

LvNotch signaling plays a dual role in regulating the position of the ectoderm-endoderm boundary in the sea urchin embryo.

The molecular mechanisms guiding the positioning of the ectoderm-endoderm boundary along the animal-vegetal axis of the sea urchin embryo remain largely unknown. We report here a role for the sea urchin homolog of the Notch receptor, LvNotch, in mediating the position of this boundary. Overexpression of an activated form of LvNotch throughout the embryo shifts the ectoderm-endoderm boundary more animally along the animal-vegetal axis, whereas expression of a dominant negative form shifts the border vegetally. Mosaic experiments that target activated and dominant negative forms of LvNotch into individual blastomeres of the early embryo, combined with lineage analyses, further reveal that LvNotch signaling mediates the position of this boundary by distinct mechanisms within the animal versus vegetal portions of the embryo. In the animal region of the embryo, LvNotch signaling acts cell autonomously to promote endoderm formation more animally, while in the vegetal portion, LvNotch signaling also promotes the ectoderm-endoderm boundary more animally, but through a cell non-autonomous mechanism. We further demonstrate that vegetal LvNotch signaling controls the localization of nuclear beta-catenin at the ectoderm-endoderm boundary. Based on these results, we propose that LvNotch signaling promotes the position of the ectoderm-endoderm boundary more animally via two mechanisms: (1) a cell-autonomous function within the animal region of the embryo, and (2) a cell non-autonomous role in the vegetal region that regulates a signal(s) mediating ectoderm-endoderm position, possibly through the control of nuclear beta-catenin at the boundary.

Animals↗
PubMed1986

Replacement of posterior by anterior endoderm reduces sterility in embryos from inverted eggs of Xenopus laevis.

The genital ridges of Xenopus laevis tadpoles reared from eggs kept in an inverted position contain less than 40% of the number of primordial germ cells (PGCs) of controls (Cleine & Dixon, 1985). It has been suggested that this reduction is caused by the germ cells' ectopic position in the anterior endoderm of larvae from inverted eggs, from where they may be unable to migrate into the genital ridges (Cleine & Dixon, 1985). This hypothesis is tested here by interchanging anterior and posterior endodermal grafts between pairs of inverted embryos at the early tailbud stage. Replacement of anterior by posterior endoderm has no effect but replacement of posterior by anterior endoderm increases the number of PGCs in the genital ridges and significantly reduces the proportion of sterile embryos. In a control series, in which the same type of grafting was done with normal embryos, replacement of posterior by anterior endoderm reduced the number of germ cells to almost zero, but replacement of anterior by posterior endoderm nearly doubled it. These findings are explained in terms of the distribution of the germ cells in the endoderm at the time of grafting. The results firstly show that the position of the germ cells is crucial to successful migration and secondly they support the notion that germ plasm has a determinative role during early germ cell differentiation.

Animals↗
PubMed1984

Intestinal cytodifferentiation in vitro of chick stomach endoderm induced by the duodenal mesenchyme.

The inductive action of duodenal mesenchyme on the cytodifferentiation of stomach endoderm in chick embryos was investigated in vitro with electron microscopy and immunofluorescence. Morphologically undifferentiated endoderm of the stomach of a 4-day embryo could differentiate only into a mucous secretory epithelium when cultured in the absence of mesenchyme. However, when cultivated in recombination with 6-day duodenal mesenchyme, most cells of 4-day stomach endoderm differentiated into intestinal absorptive cells possessing striated border and sucrase, and goblet cells, but not into stomach-type mucous secretory cells. In contrast, when 4-day stomach endoderm was cultured recombined with mesenchyme of embryonic digestive organs other than intestine, none of the stomach endoderm cells differentiated into intestinal epithelial cells. The competence of stomach endoderm for intestinal cytodifferentiation decreased rapidly with development, but remained until relatively later stages in the gizzard region. The present investigation demonstrates that duodenal mesenchyme can induce stomach endoderm, which has acquired the potency for self-differentiation into stomach-type epithelium, to cytodifferentiate into intestinal epithelium.

Animals↗
PubMed1996

Erythropoiesis and vasculogenesis in embryoid bodies lacking visceral yolk sac endoderm.

During mouse embryogenesis the first hematopoietic and endothelial cells form in blood islands located between layers of visceral endoderm and mesoderm in the yolk sac. The role of visceral endoderm in primitive hematopoiesis and vasculogenesis is not well understood. We have assessed the consequences of a lack of visceral endoderm on blood cell and vessel formation using embryoid bodies derived from mouse embryonic stem (ES) cells deficient in GATA-4, a transcription factor expressed in yolk sac endoderm. When differentiated in vitro, these mutant embryoid bodies do not develop an external visceral endoderm layer. We found that Gata4-/- embryoid bodies, grown either in suspension culture or attached to a substratum, are defective in primitive hematopoiesis and vasculogenesis as evidenced by a lack of recognizable blood islands and vascular channels and a reduction in the expression of the primitive erythrocyte marker epsilon y-globin. Expression of the endothelial cell transcripts FIk-1, FIt-1, and platelet-endothelial cell adhesion molecule (PECAM) was not affected in the mutant embryoid bodies. Gata4-/- ES cells retained the capacity to differentiate into primitive erythroblasts and endothelial cells when cultured in methylcellulose or matrigel. Analysis of chimeric mice, generated by injecting Gata4-/- ES cells into 8-cell stage embryos of ROSA26 transgenic animals, showed that Gata4-/- ES cells can form blood islands and vessels when juxtaposed to visceral endoderm in vivo. We conclude that the visceral endoderm is not essential for the differentiation of primitive erythrocytes or endothelial cells, but this cell layer plays an important role in the formation and organization of yolk sac blood islands and vessels.

Animals↗
PubMed2002

The deposition of suberin lamellae determines the magnitude of cytosolic Ca2+ elevations in root endodermal cells subjected to cooling.

A transient increase in cytosolic Ca2+ concentration ([Ca2+]cyt) is thought to be a prerequisite for an appropriate physiological response to both chilling and salt stress. The [Ca2+]cyt is raised by Ca2+ influx to the cytosol from the apoplast and/or intracellular stores. It has been speculated that different signals mobilise Ca2+ from different stores, but little is known about the origin(s) of the Ca2+ entering the cytosol in response to specific environmental challenges. We have utilised the developmentally regulated suberisation of endodermal cells, which is thought to prevent Ca2+ influx from the apoplast, to ascertain whether Ca2+ influx is required to increase [Ca2+]cyt in response to chilling or salt stress. Perturbations in [Ca2+]cyt were studied in transgenic Arabidopsis thaliana, expressing aequorin fused to a modified yellow fluorescent protein solely in root endodermal cells, during slow cooling of plants from 20 to 0.5 degrees C over 5 min and in response to an acute salt stress (0.333 m NaCl). Only in endodermal cells in the apical 4 mm of the Arabidopsis root did [Ca2+]cyt increase significantly during cooling, and the magnitude of the [Ca2+]cyt elevation elicited by cooling was inversely related to the extent of suberisation of the endodermal cell layer. No [Ca2+]cyt elevations were elicited by cooling in suberised endodermal cells. This is consistent with the hypothesis that suberin lamellae isolate the endodermal cell protoplast from the apoplast and, thereby, prevent Ca2+ influx. By contrast, acute salt stress increased [Ca2+]cyt in endodermal cells throughout the root. These results suggest that [Ca2+]cyt elevations, upon slow cooling, depend absolutely on Ca2+ influx across the plasma membrane, but [Ca2+]cyt elevations in response to acute salt stress do not. They also suggest that Ca2+ release from intracellular stores contributes significantly to increasing [Ca2+]cyt upon acute salt stress.

Aequorin↗
PubMed1999

How to grow a gut: ontogeny of the endoderm in the sea urchin embryo.

Gastrulation is the process of early development that reorganizes cells into the three fundamental tissue types of ectoderm, mesoderm, and endoderm. It is a coordinated series of morphogenetic and molecular changes that exemplify many developmental phenomena. In this review, we explore one of the classic developmental systems, the sea urchin embryo, where investigators from different backgrounds have converged on a common interest to study the origin, morphogenesis, and developmental regulation of the endoderm. The sea urchin embryo is remarkably plastic in its developmental potential, and the endoderm is especially instructive for its morphological and molecular responsiveness to inductive cell interactions. We start by examining and integrating the several models for the morphogenetic mechanisms of invagination and tissue elongation, the basic processes of endoderm morphogenesis in this embryo. We next critique the proposed mechanisms of inductive gene regulation in the endoderm that exemplifies a concept of modular transcriptional regulation. Finally, we end with an examination of the current molecular models to explain cell fate determination of the endoderm. Recent progress at the molecular level should soon allow us to explain the seminal experimental observations made in this embryo over a hundred years ago.

Animals↗
PubMed1979

Structure of the endodermal epithelium of the chick yolk sac during early stages of development.

The structure of the areas pellucida and vasculosa of the early chick embryo (stages 11-29) was examined by light, transmission and scanning electron microscopy. The most striking feature of the endodermal cells of these areas is the presence of large intracellular yolk drops which are characteristic of the regions in which they are found; lipid-like homogeneous drops in the area pellucida, heterogeneously composed pleomorphic drops in the mid-region of the area vasculosa and granular drops at the periphery of the area vasculosa in the region of the sinus terminalis. On morphological criteria it is postulated that granular drops may arise by direct engulfment of extracellular yolk, but this does not appear to be true for pleomorphic or homogeneous drops. Since the apical junctions between endodermal cells across the yolk sac are tight, they seal off the extraembryonic compartment from the vitelline circulation and presumably prevent intercellular passage of the yolk constituents. Thus the endodermal epithelium must mediate the transport of nutrients from the yolk mass to the developing embryo. Endodermal cells exhibit a variation across the yolk sac in the presence and number of structures associated with uptake of extracellular materials. The mid-region of the area vasculosa appears to be the most endocytotically active region with an abundance of microvilli, bristle-coated pits and vesicles and apical canaliculi and vacuoles. There is a close association between the endoderm and vitelline blood vessels and this association is maintained, as the yolk sac develops, by the formation of small vessels juxtaposed between the vascular surface of the endoderm and the walls of the large vitelline vessels.

Animals↗
PubMed1987

Radioautographic tracing of 3H-proline in the endodermal cells of the parietal yolk sac as an indicator of the biogenesis of basement membrane components.

The biogenesis of basement-membrane components was investigated in the endodermal cells of the rat parietal yolk sac in 12.5-day pregnant rats; 3H-proline was injected into conceptuses. After various time intervals, the parietal yolk sac, including endodermal cells and the associated Reichert's membrane, was removed and processed for electron-microscopic radioautography. Silver grains were counted over endodermal cell organelles and Reichert's membrane. At 2 and 5 min after 3H-proline injection, endodermal cells showed heavy labeling in rough endoplasmic reticulum (rER). Silver grain density over the rER decreased from 2 to 20 min and then remained at a plateau. Grain density was moderate over the Golgi apparatus initially but rose to a peak at 2 hr and decreased by 4 hr and later. Grain density was negligible over secretory granules at 2 and 5 min and increased moderately with time to reach a maximum at 8 hr. Thus, radioautographic peaks occurred sequentially in rER, Golgi apparatus, and secretory granules. By 4 hr and later, silver grains accumulated over Reichert's membrane. These results indicated that endodermal cells incorporated labeled proline into substances which were processed from the rER through the Golgi apparatus, transported from there to the cell surface by secretory granules, and released for export to Reichert's membrane. To clarify the nature of the exported substances, the amount of label present in proline and hydroxyproline residues after 3H-proline injection was measured in Reichert's membrane with or without the associated endodermal cells. Within the cells, 61.8% of the labeled proteins were classified as "sedentary" and 38.2% as "exportable." Of the label exported to Reichert's membrane, 66.3% consisted of type IV collagen and the rest of other basement-membrane components. The results obtained with this model suggest that basement-membrane proteins, including type IV collagen, are elaborated by the associated cells through the classical pathway: rER-Golgi apparatus-secretory granules.

Animals↗
PubMed1978

Differentiation and migration of endoderm in the rat and mouse at implantation.

The initial differentiation of endoderm at the time of onset of implantation, and the subsequent rapid differentiation of visceral and parietal endoderm were studied in the rat and mouse. Transmission electron microscopy illustrates the reorientation and loosening of embryonic cell mass cells during implantation, as well as cytological evidence that endoderm cells have differentiated. Using scanning electron microscopy, parietal endoderm consists of individual stellate cells with numerous peripheral branching filopodia. As these cells migrate abembryonically, the rest of the embryonic cell mass becomes recompacted. The visceral endoderm proliferates and forms a columnar epithelium which has the cytological characteristic of an absorptive epithelium and is able to ingest exogenous proteins. Thus, by 24 hours after implantation, the two endodermal derivatives have assumed widely diverse shapes and different types of associations and rates of replication, and are probably performing different functions.

Animals↗
PubMed2002

Deficits in the posterior pharyngeal endoderm in the absence of retinoids.

Recent studies have shown that the pharyngeal endoderm plays a critically important role in directing the development of the pharyngeal region of the vertebrate embryo. We have, however, had few insights into how the pharyngeal endoderm itself is patterned. Recently, several studies have suggested that retinoic acid is required for the development of the pharyngeal endoderm. To study this proposal in greater depth, we have examined the development of the pharyngeal endoderm in the absence of retinoid signalling, by using the vitamin A- deficient (VAD) quail model system. We find in early stages that, in the absence of retinoids, this territory extends further caudally than normal. Furthermore, as development proceeds, we find that the first pouch invariably forms, that the second pouch is abnormal, and that the third and fourth pharyngeal pouches never form. We do find, however, that dorsoventral patterning of the pharyngeal endoderm is unaffected. Finally, we have examined the expression patterns of RALDH2 before and during early development of the pharyngeal pouches. We find that this enzyme is expressed adjacent to the pharyngeal endoderm in tissues around the regressing anterior intestinal portal and that from stage 12 onward its anterior limit of expression lies at the level of the second pouch. This finding helps explain why the first pouch always forms in the absence of retinoids, and why defects are seen starting with the second and most evidently in the caudal pouches.

Aldehyde Oxidoreductases↗
PubMed2006

Genomic profiling of mixer and Sox17beta targets during Xenopus endoderm development.

The transcription factors Mixer and Sox17beta have well-characterized roles in endoderm specification during Xenopus embryogenesis. In order to more thoroughly understand the mechanisms by which these endodermal regulators act, we expressed Mixer and Sox17beta in naïve ectodermal tissue and, using oligonucleotide-based microarrays, compared their genomic transcriptional profile to that of unaffected tissue. Using this approach, we identified 71 transcripts that are upregulated by Mixer or Sox17beta, 63 of which have previously uncharacterized roles in endoderm development. Furthermore, an in situ hybridization screen using antisense probes for several of these clones identified six targets of Mixer and/or Sox17beta that are expressed in the endoderm during gastrula stages, providing new and regional markers of the endoderm. Our results contribute further insight into the functions of Mixer and Sox17beta and bring us closer to understanding at the molecular level the pathways that regulate endoderm development.

Animals↗
PubMed2006

Tg(Afp-GFP) expression marks primitive and definitive endoderm lineages during mouse development.

Alpha-fetoprotein (Afp) is the most abundant serum protein in the developing embryo. It is secreted by the visceral endoderm, its derivative yolk sac endoderm, fetal liver hepatocytes, and the developing gut epithelium. The abundance of this protein suggested that Afp gene regulatory elements might serve to effectively drive reporter gene expression in developing endodermal tissues. To this end, we generated transgenic mouse lines Tg(Afp-GFP) using an Afp promoter/enhancer to drive expression of green fluorescent protein (GFP). Bright GFP fluorescence allowed the visualization, in real time, of visceral endoderm, yolk sac endoderm, fetal liver hepatocytes, and the epithelium of the gut and pancreas. Comparison of the localization of green fluorescence with that of endogenous Afp transcripts and protein indicated that the regulatory elements used to generate these mouse lines directed transgene expression in what appeared to be all Afp-expressing cells of the embryo, but only in a subset of fetal liver cells. The bright GFP signal permitted flow cytometric analysis of fetal liver hepatocytes. These mice represent a valuable resource for live imaging as well as identification, quantitation, and isolation of cells from the primitive and definitive endoderm lineages of the developing mouse embryo.

Animals↗
PubMed2001

An enhancer sequence directs LacZ expression to developing pharyngeal endoderm in transgenic mice.

The murine Hoxc-6 homeobox gene comprises three exons with two distinct promoters (PRI and PRII) located 9 kb apart. To characterise the PRII promoter, a region 3 kb upstream of the transcription start site was sequenced, and an Antananapedia-like consensus binding sequence was found (Coletta et al., 1991). A LacZ reporter gene construct, containing three copies of this sequence, directs highly specific expression in cells forming pharyngeal endoderm in transgenic mice. Expression was first detected in a few individual anterior endoderm cells at E7.5, which increase in number up to E9.5, where expression was clearly visible in the pharyngeal endoderm. Expression of the endodermal genes HNF3beta, Pax-9, Shh, and Nkx2.5 showed colocalization with the LacZ-positive cells in the foregut and pharyngeal endoderm. This novel enhancer provides a means of tracking the morphogenetic movement of endodermal cells fated to form the foregut.

Animals↗
PubMed1995

Autonomous endodermal determination in Xenopus: regulation of expression of the pancreatic gene XlHbox 8.

In neural plate stage Xenopus embryos, XlHbox 8 expression marks anterior endodermal cells fated to develop into pancreas/duodenum, and expression continues in adult pancreas in exocrine duct, acinar, and islet cells. Here, XlHbox 8 is used as a marker in experiments addressing the mechanisms of early endodermal patterning, particularly with respect to the role of specific polypeptide growth factors. When mesoderm-free vegetal explants (VEs) from early blastula stage embryos are cultured in isolation, XlHbox 8 expression develops autonomously in the dorsal region, strongly suggesting that endodermal region-specific determination occurs before MBT. Data from microinjection experiments using RNA encoding the activin and FGF dominant negative receptors and growth factor treatments of isolated VEs suggest that activin positively regulates XlHbox 8 expression, whereas bFGF is a potent negative regulator. Moreover, bFGF induces mesodermal marker expression in VEs. This suggests that the early endodermal determination state is plastic and that elevated levels of bFGF may convert vegetal (endodermal) cells into mesoderm. We propose a model for XlHbox 8 regulation in which an early signal from the Nieuwkoop center (whose eventual fate is endoderm) predisposes dorsovegetal cells for autonomous XlHbox 8 expression, in an area of high local activin (or activin-like) ligand concentration, and low relative concentrations of bFGF.

Activins↗
PubMed1996

Synergistic effects of Vg1 and Wnt signals in the specification of dorsal mesoderm and endoderm.

In amphibians, dorsoventral asymmetry is established by cortical rotation, a cytoplasmic rearrangement in the egg which activates a dorsal determinant on one side of the zygote. This determinant has been proposed to be either Vgl, an endodermally derived molecule that can directly induce ectoderm to form dorsal mesoderm, or a member of the Wnt family, which patterns the ectoderm such that it forms dorsal mesoderm in response to ventral inductive signals. In this study, we have investigated whether the endogenous dorsal determinant(s) functions as a direct inducer of dorsal mesoderm (Vg1-like) or whether it acts to pattern the response of ectoderm to inductive signals (Wnt-like). We report here that cortical rotation enhances both the dorsal-inductive activity of endodermal cells and the response of ectodermal cells to endogenous inductive signals and that both of these activities are required for notochord induction in ectoderm/endoderm recombinants. While ectopically expressed Xwnt-8b can substitute for the dorsalizing signals activated in either ectoderm or endoderm, and can allow notochord formation in recombinants, Vg1 alone is not sufficient to induce notochord in ectodermal explants in the absence of signals activated by cortical rotation. Coexpression of Xwnt-8b along with Vg1 restores ectodermal competence to form notochord. Finally, in endodermal explants, ectopically expressed Xwnt-8b, but not Vg1, can divert the fate of ventral endodermal cells along a dorsal pathway. Thus, while Vg1 is most likely required for induction of mesoderm in vivo, our data suggest that a maternal Wnt-like signal acts synergistically with Vg1 to specify a dorsal fate not only in the mesoderm, but also in the endoderm.

Animals↗