PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “inner ectoderm”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 109 records · Page 6Linked to original sources
PubMed1993

Fibroblast growth factor-mediated growth regulation and receptor expression in embryonal carcinoma and embryonic stem cells and human germ cell tumours.

FGFs have been implicated in the induction of mesoderm in amphibian development and are present in the mouse embryo at stages that would be appropriate for a similar function in mammals. Primitive ectoderm would then be the target tissue. We have now changes in the expression of receptors for FGFs during the differentiation of embryonal carcinoma (EC) and embryonic stem (ES) cells from the mouse. These cells resemble those of the inner cell mass and later primitive ectoderm. On Northern blots of mRNA from undifferentiated cells, transcripts for FGF R1, R2 and R3 are expressed. All are upregulated during differentiation of ES cells and are upregulated or remain constant as EC cells differentiate. FGF R4 is only expressed after differentiation to derivatives resembling parietal endoderm. By contrast in human EC cells, FGF R2 is downregulated during differentiation, FGF R1 and FGF R3 are unchanged and FGF R4 is expressed before and after differentiation. In both human and mouse EC cells three members of the FGF family (a FGF, b FGF and k FGF, also known as FGFs 1,2 and 4) are mitogenic in serum-free medium and one (KGF or FGF 7) appears to have no effect on growth although cellular morphology is altered. Differences between human and mouse cells are primarily in the effects of heparin on the FGF-induced response.

Animals↗
PubMed2006

Gata3 is required for early morphogenesis and Fgf10 expression during otic development.

Inner ear develops from an induced surface ectoderm placode that invaginates and closes to form the otic vesicle, which then undergoes a complex morphogenetic process to form the membranous labyrinth. Inner ear morphogenesis is severely affected in Gata3 deficient mouse embryos, but the onset and basis of the phenotype has not been known. We show here that Gata3 deficiency leads to severe and unique abnormalities during otic placode invagination. The invagination problems are accompanied often by the formation of a morphological boundary between the dorsal and ventral otic cup and by the precocious appearance of dorsal endolymphatic characteristics. In addition, the endolymphatic domain often detaches from the rest of the otic epithelium during epithelial closure. The expression of several cell adhesion mediating genes is altered in Gata3 deficient ears suggesting that Gata3 controls adhesion and morphogenetic movements in early otic epithelium. Inactivation of Gata3 leads also to a loss of Fgf10 expression in otic epithelium and auditory ganglion demonstrating that Gata3 is an important regulator of Fgf-signalling during otic development.

Animals↗
PubMed2001

Origins of inner ear sensory organs revealed by fate map and time-lapse analyses.

The inner ear develops from a simple ectodermal thickening called the otic placode into a labyrinth of chambers which house sensory organs that sense sound and are used to maintain balance. Although the morphology and function of the sensory organs are well characterized, their origins and lineage relationships are virtually unknown. In this study, we generated a fate map of Xenopus laevis inner ear at otic placode and otocyst stages to determine the developmental origins of the sensory organs. Our lineage analysis shows that all regions of the otic placode and otocyst can give rise to the sensory organs of the inner ear, though there were differences between labeled quadrants in the range of derivatives formed. A given region often gives rise to cells in multiple sensory organs, including cells that apparently dispersed from anterior to posterior poles and vice versa. These results suggest that a single sensory organ arises from cells in different parts of the placode or otocyst and that cell mixing plays a large role in ear development. Time-lapse videomicroscopy provides further evidence that cells from opposite regions of the inner ear mix during the development of the inner ear, and this mixing begins at placode stages. Lastly, bone morphogenetic protein 4 (BMP-4), a member of the transforming growth factor beta (TGF-beta) family, is expressed in all sensory organs of the frog inner ear, as it is in the developing chicken ear. Inner ear fate maps provide a context for interpreting gene expression patterns and embryological manipulations.

Animals↗
PubMed1998

Apoptosis in the lens anlage of the heritable lens aplastic mouse (lap mouse).

Adult homozygous lap mice show various eye abnormalities, such as aphakia, retinal disorganization, and dysplasia of the cornea and anterior chamber. In the fetal eye of a homozygous lap mouse, the lens placode seems to develop normally. However, the lens vesicle progresses abnormally to form a mass of cells without a cavity, and the mass vanishes soon afterward. We examined cell death in the lens anlage of this mutant. The lens anlagen of homozygous lap and normal mice from days 10 to 12 of gestation were observed by light microscopy after DNA end-labeling by immunohistochemistry and by transmission electron microscopy. By light microscopy, a slight frequency of cell death was detected in the lens anlage encircling the surface ectoderm and in the anlage or in the anlage of both homozygous lap mice and normal mice at day 10 of gestation. Cell death was seen in the lens anlage encircling the surface ectoderm in the normal mouse and sporadically in the anlage of the homozygous lap mouse at day 10.5 of gestation. Cell death was visible at the area of the lens vesicle attached to the surface ectoderm and encircling the surrounding surface ectoderm in the normal mouse, and in the lens anlage encircling the surface ectoderm and the apex areas of the lens anlage in the homozygous lap mouse at day 11 of gestation. At day 12 of gestation, almost no cell death was observed in the lens anlage of the normal mouse. However, extensive areas of cell death were still seen in the lens anlage at its apex, at the inner region, and encircling the surface ectoderm in the homozygous lap mouse. Electron microscopic observation showed that the dead cells observed in the lens anlagen by light microscopy in normal and lap mice are the result of apoptosis. In lap mice, cells with cytoplasmic condensation were observed mainly at days 10 and 10.5 of gestation. Many apoptotic bodies which had been phagocytosed by adjacent cells were seen predominantly at day 11 of gestation. At day 12 of gestation, apoptotic bodies phagocytosed by adjacent cells, which were seen at day 11, were still predominant, but there were more apoptotic bodies per cell and more digested apoptotic bodies than at day 11. These results indicate that cell death, resulting from apoptosis is involved in the disappearance of the lens anlage of lap mice.

Animals↗
PubMed1998

Morphological and quantitative studies in the otic region of the neural tube in chick embryos suggest a neuroectodermal origin for the otic placode.

Careful histological observation of the development of the anlage of the inner ear in chicken embryos led us to question the traditional view of otic placode (OP) formation. First, morphological studies in the cephalic region carried out on stages preceding the appearance of the placodal epithelium revealed that the medial placodal cells are continuous temporally and spatially with cells belonging to the neural fold (NF). Second, both the formation of the basal lamina between the dorsal region of the neural tube (NT) and ectoderm and the pattern of formation of the neural crest present distinctive characteristics between otic levels and regions located anteriorly and posteriorly. Third, numerical comparisons of parameters for the NT and the OP between different levels of the rhombencephalon allowed us to assign a differential behaviour in the growth pattern of the otic region. These results indicated that the medial part of the OP is not derived from already independent ectoderm that increases in thickness under the influence of the NT (as previously accepted) but that it develops directly from the NFs. Although we do not exclude other possibilities, we propose that at least a proportion of the OP cells originate directly from cells committed to be neural crest. After this incorporation, basal laminal formation would delimit the NT from the OP without transition of the otic cells to ectoderm. This hypothesis would imply that part of the otic cells originate directly from neuroepithelial cells having a neuroectodermal (rather than the previously established ectodermal) origin.

Animals↗
PubMed1996

Inductive processes leading to inner ear formation during Xenopus development.

This study examines the spatial and temporal attributes of inner ear induction in Xenopus embryos. These results are compared to recent experiments concerning lens induction to assess whether head sensory structures share common ontogenetic features. Ectoderm from different regions and stages was transplanted to the presumptive ear region of hosts of either early (neural plate) or late (neural tube) stages. Explants of the presumptive ear ectoderm were also taken from embryos at these stages to establish the time of otic ectoderm specification. We find that ectodermal competence for otic vesicle formation extends through neural plate stages, far longer than for lens formation. Otic vesicle specification occurs substantially earlier, at neural plate stages, than lens specification. Competent ectoderm forms otic vesicles in a high fraction of cases when exposed to the ear-inducing environment of either neural plate stages or neural tube stages, a result which contrasts with lens induction where the neural tube stage embryo provides a much weaker inducing environment than earlier stages. Otic vesicles induced in neural tube stage hosts are primarily in contact with presumptive hindbrain, suggesting that this neural tissue may be sufficient for otic vesicle induction. These studies reveal overall similarities between lens and inner ear induction, but sufficient differences to propose that some facets of determination of these sensory tissues may occur by independent mechanisms and not via a common developmental state.

Animals↗
PubMed1982

Effects of fluorodeoxyuridine on the developing inner ear of the rat.

The inner ear in rats develops from the surface ectoderm on day 8 of a 22-day gestational period. Labeled thymidine incorporation studies have indicated that in the developing inner ear most of the cells undergo terminal mitosis between gestational days 13 and 15. During this period the developing inner ear would be particularly vulnerable to environmental hazards. To test this hypothesis, pregnant rats were given a single intraperitoneal injection of 5-fluoro-2'-deoxyuridine (FUdR), an antimitotic substance, on gestational days 12 to 16. The rats also received one injection of 3H-thymidine 1 h prior to the removal of the fetuses. The animals were killed after various time intervals following the treatment, and the otocysts or inner ears were prepared for morphologic observations and biochemical assays. The cells in the inner ear of rats exposed to FUdR exhibited pyknotic nuclei and chromatolytic degeneration, and they eventually died. By 4 h after the administration of FUdR, pyknotic nuclei were seen in the antiluminal zone of the otic epithelium, and there was a substantial decrease in the number of the otic cells. This decline in cell number was seen until 24 h after treatment. However, the inner ears from the fetuses exposed to FUdR during gestational days 12--15 showed complete recovery from the toxic effects of the drug when examined on day 21 of gestation. The phenomenon of programmed cell death observed in the developing inner ear of the rat indicates that more cells are produced during the earlier stages of development than are required for the definitive adult structures. This phenomenon may represent an important protective feature. The redundant production of cells perhaps allows the developing otocysts to respond to an environmental stress by subtotal destruction of cells from the pool of undifferentiated cells, resulting in relatively fewer congenital anomalies of the inner ear.

Animals↗
PubMed1999

Formation of a primitive ectoderm like cell population, EPL cells, from ES cells in response to biologically derived factors.

The primitive ectoderm of the mouse embryo arises from the inner cell mass between 4.75 and 5.25 days post coitum, around the time of implantation. Positioned at a pivotal time in development, just prior to formation of the three germ layers of the embryo proper, the primitive ectoderm responds directly to the signals generated during gastrulation. We have identified a conditioned medium, MEDII, which caused the homogeneous conversion of ES cells to a morphologically distinct cell population, termed early primitive ectoderm-like (EPL) cells. EPL cells expressed the pluripotent cell markers Oct4, SSEA1 and alkaline phosphatase. However, the formation of EPL cells was accompanied by alterations in Fgf5, Gbx2 and Rex1 expression, a loss in chimaera forming ability, changes in factor responsiveness and modified differentiation capabilities, all consistent with the identification of EPL cells as equivalent to the primitive ectoderm population of the 5.5 to 6.0 days post coitum embryo. EPL cell formation could be reversed in the presence of LIF and withdrawal of MEDII, which suggested that EPL cell formation was not a terminal differentiation event but reflected the ability of pluripotent cells to adopt distinct cell states in response to specific factors. Partial purification of MEDII revealed the presence of two separable biological activities, both of which were required for the induction and maintenance of EPL cells. We show here the first demonstration of uniform differentiation of ES cells in response to biological factors. The formation of primitive ectoderm, both in vivo and in vitro, appears to be an obligatory step in the differentiation of the inner cell mass or ES cells into cell lineages of the embryonic germ layers. EPL cells potentially represent a model for the development of lineage specific differentiation protocols and analysis of gastrulation at a molecular level. An understanding of the active components of MEDII may provide a route for the identification of factors which induce primitive ectoderm formation in vivo.

Animals↗
PubMed2002

Stage- and cell-specific expression of Dnmt3a and Dnmt3b during embryogenesis.

DNA methylation is essential for development. Two DNA methyltransferases, Dnmt3a and Dnmt3b, contribute to the creation of DNA methylation patterns in embryos. We demonstrated that the Dnmt3a and Dnmt3b proteins are expressed at different stages of embryogenesis. Dnmt3b is specifically expressed in totipotent embryonic cells, such as inner cell mass, epiblast and embryonic ectoderm cells, whilst Dnmt3a is significantly and ubiquitously expressed after E10.5. The difference in the expression stages of the Dnmt3a and Dnmt3b proteins may contribute to their distinct functions during the embryogenesis.

Animals↗
PubMed1975

[Morphogenesis and structure of teleost teeth (Salmo fario L.)].

Tooth formation has been studied in the fry and adult trout (Salmo fario L.) in order to describe their structure and investigate the links between histogenetic and architectural features. Odontoblasts show typical polarized kinetics during their activity; they shrink back from the tooth wall they have elaborated, without leaving any cytoplasmic process (Tomes' fibres); so the dentine in a characteristic way lacks any cellular or canalicular inclusion, at any stage of its development. The tooth as a whole grows from an apical to basal direction; its organic matrix is formed of coarse fibres from the pulp, and fine collagenous fibres formed by the odontoblastic layer. These various fibrillar systems assume definite orientations. Mineralization was studied by fluorescent markers and microradiography. The external apical part of the tooth is hypermineralized, but its structure and pattern of deposition would make it closer to a dentinal differentiation (enameloid) than to an ectodermal enamel. The ameloblasts of the inner epithelium are high, very polarized and active cells, but their participation in tooth tissue formation has not been definitely demonstrated.

Ameloblasts↗
PubMed2004

Fgf9 signaling regulates inner ear morphogenesis through epithelial-mesenchymal interactions.

The mammalian inner ear comprises the cochleovestibular labyrinth, derived from the ectodermal otic placode, and the encasing bony labyrinth of the temporal bone. Epithelial-mesenchymal interactions are thought to control inner ear development, but the modes and the molecules involved are largely unresolved. We show here that, during the precartilage and cartilage stages, Fgf9 is expressed in specific nonsensory domains of the otic epithelium and its receptors, Fgfr1(IIIc) and Fgfr2(IIIc), widely in the surrounding mesenchyme. To address the role of Fgf9 signaling, we analyzed the inner ears of mice homozygous for Fgf9 null alleles. Fgf9 inactivation leads to a hypoplastic vestibular component of the otic capsule and to the absence of the epithelial semicircular ducts. Reduced proliferation of the prechondrogenic mesenchyme was found to underlie capsular hypoplasticity. Semicircular duct development is blocked at the initial stages, since fusion plates do not form. Our results show that the mesenchyme directs fusion plate formation and they give direct evidence for the existence of reciprocal epithelial-mesenchymal interactions in the developing inner ear. In addition to the vestibule, in the cochlea, Fgf9 mutation caused defects in the interactions between the Reissner's membrane and the mesenchymal cells, leading to a malformed scala vestibuli. Together, these data show that Fgf9 signaling is required for inner ear morphogenesis.

Animals↗
PubMed1999

Endoderm differentiation and inductive effect of activin-treated ectoderm in Xenopus.

When presumptive ectoderm is treated with high concentrations of activin A, it mainly differentiates into axial mesoderm (notochord, muscle) in Xenopus and into yolk-rich endodermal cells in newt (Cynops pyrrhogaster). Xenopus ectoderm consists of multiple layers, different from the single layer of Cynops ectoderm. This multilayer structure of Xenopus ectoderm may prevent complete treatment of activin A and subsequent whole differentiation into endoderm. In the present study, therefore, Xenopus ectoderm was separated into an outer layer and an inner layer, which were individually treated with a high concentration of activin A (100 ng/mL). Then the differentiation and inductive activity of these ectodermal cells were examined in explantation and transplantation experiments. In isolation culture, ectoderm treated with activin A formed endoderm. Ectodermal and mesodermal tissues were seldom found in these explants. The activin-treated ectoderm induced axial mesoderm and neural tissues, and differentiated into endoderm when it was sandwiched between two sheets of ectoderm or was transplanted into the ventral marginal zone of other blastulae. These findings suggest that Xenopus ectoderm treated with a high concentration of activin A forms endoderm and mimics the properties of the organizer as in Cynops.

Activins↗
PubMed1997

Each member of the Id gene family exhibits a unique expression pattern in mouse gastrulation and neurogenesis.

We have performed a detailed comparative in situ hybridization analysis to examine the patterns of expression of all the members of the Id gene family (Id1-4) during murine gastrulation and neurogenesis. During gastrulation, both Id1 and Id3 are expressed in the tissues derived from the inner cell mass from 5.5 dpc onward, whereas Id2 is expressed in tissues derived from trophoblasts. Id4 expression is absent during this period of development. Embryonic Id1 messages are detected during gastrulation on the proximal side of the embryonic ectoderm, which is the border between the embryo proper and the extraembryonic tissues, and the expression of Id3 is found throughout the entire embryo proper. This unique pattern of expression of the different members of the Id family suggests a nonredundant role for these genes in antagonizing the activity of bHLH transcription factors during very early mouse development. During neurogenesis, the expression of each member of the Id family is present in an unique pattern along the dorsal-ventral axis of the neural tube: In the early stages of spinal cord development, both Id1 and Id2 are expressed in the roof plate, whereas Id3 is expressed both in the roof and the floor plates. As development progresses, the expression of both Id1 and Id3 is detected in the dividing neuroblasts, whereas Id2 and 4 are expressed in presumptive neurons which are undergoing maturation. The expression patterns of all the members of the Id gene family persist throughout the entire CNS, both in the spinal cord and in the brain. In addition, the characteristic expression of Id2 and Id4 in more mature neurons is reiterated both in the PNS and in the neurons of some of the sensory organs. These data suggest that the expression of different subgroups of the Id gene family may have different physiological consequences and thereby contributes in unique ways to specify the differentiation state of neuronal cells during development.

Animals↗
PubMed1992

Regional expression of three homeobox transcripts in the inner ear of zebrafish embryos.

The inner ear of all jawed vertebrates arises from the epithelium of the otic vesicle and contains three semicircular canals, otoliths, and sets of sensory neurons, all positioned precisely within the cranium to detect head orientation and movement. The msh-C gene and two new homebox genes, msh-D and a gene related to distal-less, dlx-3, are each expressed in distinct regions of the otic vesicle during its early development in zebrafish embryos. Cells in the ectoderm express dlx-3 before induction of the otic vesicle, suggesting that dlx-3 has an early function in this process. Later, cells aligned with the future axes of the semicircular canals specifically express either dlx-3 or msh-D. Even later, sensory hair cells express msh-C and msh-D, while other cells of the epithelium express dlx-3. The early expression of these genes could specify the orientation and morphogenesis of the inner ear, whereas their later expression could specify the fates of particular cell types.

Amino Acid Sequence↗
PubMed1998

A key function for alphav containing integrins in mesodermal cell migration during Pleurodeles waltl gastrulation.

During cleavage of Pleurodeles waltl amphibian embryos, inner cells of the blastocoel roof (presumptive ectodermal and mesodermal cells) organize a fibrillar extracellular matrix (ECM) containing fibronectin on their basal surface by a beta1-integrin-dependent process. This matrix is used as a migratory substrate by mesodermal cells during gastrulation. While alpha5beta1 integrin is expressed on both ectodermal and mesodermal cell surface, we have shown previously that alphav containing integrins are essentially restricted to the surface of mesodermal cells (Alfandari, D., Whittaker, C. A., DeSimone, D. W., and Darribère, T., Dev. Biol. 170, 249-261, 1995). To investigate the function of alphav integrins during gastrulation, we have generated a function blocking antibody directed against the extracellular domain of the Pleurodeles integrin alphav subunit. The antibody did not prevent fibronectin fibril formation, whereas an antibody against the alpha5beta1 integrin did. When injected into the blastocoel, the antibody against integrin alphav subunit perturbed gastrulation and further development in a stage-dependent manner. Developmental defects were correlated to an abnormal positioning of the mesoderm layer. In vitro, the antibody blocked spreading of mesodermal cell to fibronectin or blastocoel roof ECM but not their attachment. In contrast, the antibody directed against the alpha5beta1 integrin inhibited both cell attachment and spreading to the same substrates. We propose that the alpha5beta1 integrin is required for fibronectin assembly into fibrils and mesodermal cell attachment to the blastocoel roof ECM, while the alphav containing integrins are necessary for cell spreading, and possibly migration, on this complex network.

Animals↗
PubMed1995

Development of Reichert's membrane in the early mouse embryo.

Although the composition of Reichert's membrane, a thick multilayered basement membrane between the parietal endoderm cells and the trophoblast cells of rodents, has often been investigated, the site of its production remains a subject of controversial discussion. In particular, the role of the trophoblast cells is unclear. In the present work we examined the initial development of Reichert's membrane in the early mouse embryo, using glutaraldehyde fixation with tannic acid. In the early blastocyst the occurrence of a tannic-acid-positive layer located at the inner surface of the mural trophoblast indicated the onset of basement membrane formation by the trophoblast cells. In the peri-implantation phase, this basement membrane extended into lateral areas of the inner cell mass separating the newly differentiated ectoderm and endoderm cells from each other. In these lateral regions, where the recently formed primitive endoderm cells had been attached to the monolayered basement membrane of the mural trophoblast cells, followed by an apposition of basement membrane material, probably synthesized by primitive endoderm cells, along this primary membrane.

Animals↗
PubMed2005

In situ analysis of Raidd-beta-galactosidase fusion gene expression in transgenic mouse midgestation embryos.

Apoptosis and differentiation are tightly intertwined processes occurring at organ formation and remodelling during embryonic development. RAIDD (receptor-interacting protein [RIP]-associated ICH-1/CED-3-homologous protein with a death domain), a dual-domain adaptor protein has been shown to mediate the recruitment of CASPASE-2 to tumour necrosis factor receptor-1 (TNF-R1) signalling complex through RIP kinase. However, Raidd overexpression studies suggest that apart from the established role in apoptosis, Raidd may have an additional function in cell differentiation. In this study, we could not generate Raidd null adult mice suggesting that lack of function of Raidd might be embryonic lethal. Thus, to elucidate the role of Raidd during mouse embryogenesis when the processes of organogenesis are most dynamic, we studied the Raidd expression pattern in midgestation mouse embryos. We generated Raidd+/- transgenic mice with a reporter transgene encoding the bacterial Beta-galactosidase (beta-gal) under the control of Raidd promoter. During the midgestation period (E8.5-E12.5), Raidd is expressed in developing organs derived from the ectoderm such as lens, structures of the inner ear and the fourth brain ventricle in regions where differentiation takes place implicating Raidd role in this process. In addition, Raidd expression was found in developing mesenchyme organs like heart and kidney and in the endothelial lining of the midgut at the time when profound morphological changes take place in these organs. In developing heart and kidney Raidd expression patterns overlapped with known zones of cell death suggesting Raidd may be involved in apoptosis-mediated remodelling. The observed lethality of mice targeted at both Raidd alleles and Raidd expression patterns during midgestation period strongly suggest that Raidd plays an important role in mammalian development.

Adaptor Proteins, Signal Transducing↗