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Scanning electron microscopic observations on the 9-day opossum (Didelphis virginiana) embryo.

All three germ layers are present in the opossum embryo by the 9th prenatal day. The embryo proper is part of, and continuous with, the remainder of the chorionic wall. The wall of the yolk sac-chorion away from the embryo consists only of an outer covering of ectoderm and an inner layer of endoderm. Ectodermal cells covering the neural folds have dome-shaped apices and often show large, bleb-like expansions. Microvilli are short and few in number. The apical surfaces of ectodermal cells that overlie the parietal mesoderm are relatively smooth and show scattered, short microvilli that tend to be concentrated at cell junctions. The apices of ectodermal cells that cover the extraembryonic region are more rounded, and the cells balloon from the surface. Each cell shows abundant elongate microvilli and occasional cytoplasmic blebs. Endodermal cells that line the chorion and form the third (innermost) layer of the embryo are similar in their surface morphology.

Animals↗

Development of apical-surface structures of mouse otic placode.

In 8.0 gestation-day embryos, a central cilium and microvilli were present on the apical surface of the cells of the presumptive otic placode and other ectoderm regions as well. The cilium at this stage lacked a central pair of fibres and was regarded as a primitive cilium with 9+0 composition. The microvilli gained in length and density of distribution as soon as the otic placode began to invaginate in 8.5-d. embryos. With further development in 9.5-11.0-d. embryos, they took on a regular distribution pattern. Narrowing and concomitant bulging out appeared in the cells along the neck of the otic invagination in 8.5-d. embryos. Marked regional differences also occurred in the apical-surface structures of the cells, particularly in the relatively more advanced form of the embryos. Kinocilia of the adult vestibular sensory cells were found to lack a continuous central pair of fibres, resembling the apical cilia of the otic placode. This finding seems to suggest that a vestibular kinocilium represents a direct descendant from the primordial cilium, which generally emerges from the primordial ectodermal cells and is entirely lost from the keratinizing ectoderm in the later development.

Animals↗

Competence of cranial ectoderm to respond to Fgf signaling suggests a two-step model of otic placode induction.

Vertebrate craniofacial sensory organs derive from ectodermal placodes early in development. It has been suggested that all craniofacial placodes arise from a common ectodermal domain adjacent to the anterior neural plate, and a number of genes have been recently identified that mark such a 'pre-placodal' domain. However, the functional significance of this pre-placodal domain is still unclear. In the present study, we show that Fgf signaling is necessary and sufficient to directly induce some, but not all, markers of the otic placode in ectoderm taken from the pre-placodal domain. By contrast, ectoderm from outside this domain is not competent to express otic markers in response to Fgfs. Grafting naïve ectoderm into the pre-placodal domain causes upregulation of pre-placodal markers within 8 hours, together with the acquisition of competence to respond to Fgf signaling. This suggests a two-step model of craniofacial placode induction in which ectoderm first acquires pre-placodal region identity, and subsequently differentiates into particular craniofacial placodes under the influence of local inducing signals.

Animals↗

[The determination of ectodermal derivatives in various species of amphibia].

The process of labyrinth determination has been studied in amphibians (three Urodela and seven Anura species) using homoplastic transplantation of ear ectoderm, containing labyrinth material onto the abdominal wall of embryos of the same stage of development. The stage of appearance of organ-specific properties in ear ectoderm was determined and the increase of these properties in the course of development was observed. The frequency of ear vesicles formation, the level of their differentiation and their size served as criteria. These criteria allow to align the studied species into a row, where organ-specific properties appear earlier and most completely in representatives of Ranidae family and in Bufo viridis, and weakest, in smooth newt. A comparison of properties of labyrinth material and other areas of ectoderm allowed to conclude that specific differences in determination of different ectodermal primordia are based on specific peculiarities of the whole ectoderm. The appearance of these differences can be explained by the shift in the beginning of gastrulation towards later stages of cleavage during the evolution of amphibians.

Amphibians↗

Foxi2 and Sox3 are master regulators controlling ectoderm germ layer specification.

In vertebrates, germ layer specification represents a critical transition where pluripotent cells acquire lineage-specific identities. We identify the maternal transcription factors Foxi2 and Sox3 to be pivotal master regulators of ectodermal germ layer specification in Xenopus. Ectopic co-expression of Foxi2 and Sox3 in prospective endodermal tissue induces the expression of ectodermal markers while suppressing mesendodermal markers. Transcriptomics analyses reveal that Foxi2 and Sox3 jointly and independently regulate hundreds of ectodermal target genes. During early cleavage stages, Foxi2 and Sox3 pre-bind to key cis-regulatory modules (CRMs), marking sites that later recruit Ep300 and facilitate H3K27ac deposition, thereby shaping the epigenetic landscape of the ectodermal genome. These CRMs are highly enriched within ectoderm-specific super-enhancers (SEs). Our findings highlight the pivotal role of ectodermal SE-associated CRMs in precise and robust ectodermal gene activation, establishing Foxi2 and Sox3 as central architects of ectodermal lineage specification.

Ep300↗

Cell fate specification in the inner ear.

From its origin as a single ectodermal patch, the inner ear becomes a labyrinth of chambers housing six to eight sensory organs. Along the way, specific cell fates are realized. The secrets underlying these cell fate specifications are beginning to be revealed through the application of several molecular-genetic approaches. Recent papers describing such approaches have included gene expression studies in the early otic epithelium and inner ear sensory epithelia. large-scale screens of zebrafish mutants to identify ear defects, and targeted gene perturbations of neurotrophins. of their receptors or of the Brn-3.1 transcription factor in mice.

Animals↗

Identification of a biological activity that supports maintenance and proliferation of pluripotent cells from the primitive ectoderm of the mouse.

Pluripotent cell development in the mammalian embryo results in the sequential formation of several developmentally distinct populations, inner cell mass, primitive ectoderm, and the primordial germ lineage. Factors within medium conditioned by HepG2 cells (MEDII) have been implicated in the formation and maintenance of primitive ectoderm from inner cell mass cells both in vitro and in vivo. Here we demonstrate that MEDII, but not LIF, is able to support the maintenance and proliferation in culture of pluripotent cells derived from primitive ectoderm formed in vitro or during embryonic development. This distinguishes primitive ectoderm and inner cell mass (ICM) on the basis of cytokine responsiveness and validates the biological activity proposed for factors within MEDII in primitive ectoderm establishment and maintenance. Further, it potentially provides an alternative technology for the isolation of pluripotent cells from the mammalian embryo.

Animals↗

A theory on the embryogenesis of oculo-auriculo-vertebral (Goldenhar) syndrome.

Oculo-auriculo-vertebral (OAV) syndrome is made up of anomalies, mainly of first and second branchial arch derivatives. Characteristic features include structural malformations of the external and middle ears, face, and jaw. It has been previously suggested that hemorrhage involving the first and second branchial arches causes hypoplasia and malformation of the face and auricle, but this theory cannot explain the multisystemic and protean manifestations of this disease. The theory set forth describes the cutaneous, facial, vertebral, and systemic anomalies in the OAV spectrum as a result of ectodermal nondisjunction early in development with subsequent mesodermal tethering. A subgroup of OAV may therefore be a disorder of ectodermal nondisjunction involving the otic placode similar to the spectrum of diseases such as occult spinal dysraphism that is associated with the same mechanism in the embryonic neuraxis. This would imply a molecular mechanism involving cell adhesion molecules that unify the two disease processes and explain the multisystem anomalies of the OAV syndrome.

Branchial Region↗

Wnt6 marks sites of epithelial transformations in the chick embryo.

In a screen for Wnt genes executing the patterning function of the vertebrate surface ectoderm, we have isolated a novel chick Wnt gene, chick Wnt6. This gene encodes the first pan-epidermal Wnt signalling molecule. Further sites of expression are the boundary of the early neural plate and surface ectoderm, the roof of mesencephalon, pretectum and dorsal thalamus, the differentiating heart, and the otic vesicle. The precise sites of Wnt6 expression coincide with crucial changes in tissue architecture, namely epithelial remodelling and epithelial-mesenchymal transformation (EMT). Moreover, the expression of Wnt6 is closely associated with areas of Bmp signalling.

Amino Acid Sequence↗

[Rostral curvature of the proximal visceral segment--a previously unknown embryonal movement].

Before the development of the chondrocranium within the head region of the human embryo the following different, so far unknown, tissue shifts are demonstrable: Because of the dorsal brain- sheats of the rostral regions of the brain (mes- and diencephalon) don't have yet blood-vessels (area avasculosa ), they are unable to increase and have to be completed by material from more caudal regions. Therefore from the middle of the 5th up to the end of the 7th week of the embryonic life the mesenchymal and ectodermal rhombencephalic brain- sheats are drawn from caudal to rostral. This becomes possible because the rhombencephalon by that passively is put into the pontine and the neck flexures, which also shift rostralwards , thus allowing the hindbrain to shorten. The proximal ends of the visceral arches I and II, where the anlagen of the temporomandibular joint and of the ear are localized, are parts of the latero-basal rhombencephalic brain- sheats . They take part in of this rostral shift. By that all their axial structures, the first branchial groove and the anlage of the auricle synchronistically undergo positional changes proving the rostral bend of the proximal region of the two visceral arches.

Brain↗

Ultrastructural development of the early rat otocyst.

The ultrastructural development and differentiation of cells forming the rat otocyst were studied from the 9th to the 13th postcoital day (PCD). The earliest stage investigated was a simple ovoid structure with a connecting stalk to the surface ectoderm. A process of programmed cellular death involving surface ectoderm, connecting stalk, and lateral otocyst wall rapidly detached the otocyst. The cells forming the otocyst were roughly columnar, the organelles were polarized; mitochondria occurred in greatest number basally and in the supranuclear area; Golgi membranes when present were supranuclear. Luminal cells had many microvilli and cilia of various lengths were detected. The shorter, incompletely formed cilia terminated in small knob-like blebs. With each day the otocysts became more complicated and the endolymphatic duct made its appearance as an evagination of the otocyst. Many more cells were seen to have cilia in various stages of development, and by the 12th PCD possibly each cell of the main otocystic cavity had a kinocilium. Growth of the otocyst due to mitosis occurred to a great extent from a single ventromedial center. Cells in mitosis, although seen at other sites, were in greatest abundance in this area; cellular involution apparently was a related function. Together the process of over-production and programmed cellular involution of supranumerary cells not lost to other causes (e.g., environmental) may represent an evolutionary advantage.

Animals↗

Vertebrate cranial placodes I. Embryonic induction.

Cranial placodes are focal regions of thickened ectoderm in the head of vertebrate embryos that give rise to a wide variety of cell types, including elements of the paired sense organs and neurons in cranial sensory ganglia. They are essential for the formation of much of the cranial sensory nervous system. Although relatively neglected today, interest in placodes has recently been reawakened with the isolation of molecular markers for different stages in their development. This has enabled a more finely tuned approach to the understanding of placode induction and development and in some cases has resulted in the isolation of inducing molecules for particular placodes. Both morphological and molecular data support the existence of a preplacodal domain within the cranial neural plate border region. Nonetheless, multiple tissues and molecules (where known) are involved in placode induction, and each individual placode is induced at different times by a different combination of these tissues, consistent with their diverse fates. Spatiotemporal changes in competence are also important in placode induction. Here, we have tried to provide a comprehensive review that synthesises the highlights of a century of classical experimental research, together with more modern evidence for the tissues and molecules involved in the induction of each placode.

Animals↗

Isolation and characterization of a near-diploid differentiated cell line from a murine teratocarcinoma that differentiates into muscle.

Cell lines corresponding to various cell lineages of the mouse embryo have been isolated from murine teratocarcinomas. Embryonal carcinoma cell lines are developmentally equivalent to the embryonic ectoderm or inner cell mass. Most of these cell lines have a modal chromosome number equal or close to 40, the normal mouse complement. However, cell lines corresponding to more advanced cell lineages (e.g., endoderm) are tetraploid or hypotetraploid and display multiple chromosomal rearrangements. This paper describes the isolation of a near-diploid differentiated cell line (LT-D) from an LT teratocarcinoma. The modal chromosome number of LT-D is 40, and this number is stable during at least 12 mo of continuous culture. LT-D cells are morphologically distinct from embryonal carcinoma cells and no longer express the SSEA-1 cell surface antigen or high alkaline phosphatase activity characteristic of embryonal carcinoma cells. LT-D cells can be induced to fuse into structures resembling myotubes. The formation of these structures is accompanied by expression of the muscle-specific isozyme of creatine phosphokinase and desmin, a muscle-specific component of intermediate filaments. Lastly, LT-D cells do not form tumors in syngenetic mice.

Alkaline Phosphatase↗

Two distinct subgroups of Group B Sox genes for transcriptional activators and repressors: their expression during embryonic organogenesis of the chicken.

Group B Sox genes, Sox1, -2 and -3 are known to activate crystallin genes and to be involved in differentiation of lens and neural tissues. Screening of chicken genomic sequences for more Group B Sox genes identified two additional genes, Sox14 and Sox21. Proteins encoded by Sox14 and Sox21 genes are similar to each other but distinct from those coded by Sox1-3 (subgroup B1) except for the HMG domain and Group B homology immediately C-proximal of the HMG domain. C-terminal domains of SOX21 and SOX14 proteins function as strong and weak repression domains, respectively, when linked to the GAL4 DNA binding domain. These SOX proteins strongly (SOX21) or moderately (SOX14) inhibited activation of delta1-crystallin DC5 enhancer by SOX1 or SOX2, establishing that Sox14 and Sox21 are repressing subgroup (B2) of Group B Sox genes. This provides the first evidence for the occurrence of repressor SOX proteins. Activating (B1) and repressing (B2) subgroups of Group B Sox genes display interesting overlaps of expression domains in developing tissues (e.g. optic tectum, spinal cord, inner ear, alimentary tract, branchial arches). Within each subgroup, most expression domains of Sox1 and -3 are included in those of Sox2 (e.g. CNS, PNS, inner ear), while co-expression of Sox14 and Sox21 occurs in highly restricted sites of the CNS, with the likely temporal order of Sox21 preceding Sox14 (e.g. interneurons of the spinal cord). These expression patterns suggest that target genes of Group B SOX proteins are finely regulated by the counterbalance of activating and repressing SOX proteins.

Amino Acid Sequence↗