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PubMed1981

In vivo and in vitro development of mouse embryos homozygous for the embryonic lethal velvet coat (Ve) mutation.

Embryos homozygous for the velvet coat mutation, Ve/Ve, were recognized at 6.5 days post coitum by the reduced size of the ectodermal portions of the egg cylinder and the loose, columnar nature of the overlying endoderm. Later in development ectoderm tissues were sometimes entirely absent. Abnormalities appeared in the ectoplacental cone at 8.5 days but trophoblast giant cells and parietal endoderm appeared unaffected. Homozygotes could not be unequivocally identified at 5.5 days nor at the blastocyst stage but were recognized in blastocyst outgrowths by poor development of the inner cell mass derivatives. It has previously been suggested that Ve may exert its action at the blastocyst stage by reducing the size of the inner cell mass, but no evidence for such a reduction was found. Most of the observations on Ve/Ve homozygotes are, however, consistent with the hypothesis that Ve exerts its action primarily on later primitive ectoderm development.

Animals↗
PubMed2005

Transforming growth factor beta 2 promotes the formation of the mouse cochleovestibular ganglion in organ culture.

The inner ear structures are derived from the otic vesicle (OV) which is formed by thickening and invagination of the otic placode of the surface ectoderm. A number of neuroblasts, which arise from epithelial cells of the otic vesicle, delaminate and differentiate into neurons of the cochleovestibular ganglion (CVG). We have found that transforming growth factor-BEta2 (Tgfbeta2 ) was expressed in the otic epithelium at the OV stages between Embryonic days (E) 9.5 and 11.5 and that anteroventrolateral localization of its expression in the OV overlapped with that of NeuroD, which is a marker of delaminating CVG precursors. The expression of TGFbeta type I and type II receptors in the otic epithelium and the nuclear localization of phosphorylated-Smad2 in both the otic epithelium and CVG suggested that TGFbeta2 signaling plays some roles in CVG formation. In order to examine the roles of TGFbeta2 in differentiation of the inner ear, otic vesicle explants of E10.5 mouse embryos were treated in vitro with TGFbeta2 or the TGFbeta type I receptor kinase inhibitor, SB431542. Addition of TGFbeta2 peptide to the culture led to Enlargement of the CVG, while the inhibitor reduced its size. These findings strongly imply that TGFbeta2 contributes to the development of the CVG in mouse embryos.

Animals↗
PubMed1976

Three-dimensional anatomy of the 8-day mouse concepts: a study by scanning electron microscopy.

The three-dimensional anatomy of the 8-day mouse concepts was studied by scanning electron microscopy aided by microdissection within the microscope specimen chamber. Attention was given to the relationship of the extra-embryonic membranes and their subtended compartments and particular emphasis was placed on the 'inverted' condition of the embryo at this stage of development. The main points brought forth in this study are: (1) the five basic brain segments are discernible on the basis of surface contour; (2) the cervical fold, extending from the ventrum of the metencephalon to the somatopleure, forms a partition which separates the branchial region from the rest of the amniotic space; (3) the procephalic membrane bifurcates in a vertical plane to form the splanchnopeure and somatopleure lateral to the forebrain, and it bifurcates horizontally to form the dorsal and ventral coverings of the pericardial coelom; (4) the anttrum of the pericardial-peritoneal canal opens into the lateral coelom posterior to the cervical fold; (5) the midgut of the embryo is delineated laterally by longitudinal grooves connecting the foregut and hindgut antra; (6) embryonic ectoderm in the neural-fold region is formed by a single layer of pseudostratified columnar cells; (7) the allantois is hollow near its base and the inner surface is formed by a discontinuous layer of squamous cells; (8) blood islands in the extra-embryonic mesoderm form a ring of bulges around the middle of the exocoel. Other structures such as the ectoplacental cavity, the ectoplacental cone and the parietal capsule are also described.

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PubMed2000

Cellular basis of gastrulation in the sand dollar Scaphechinus mirabilis.

The processes of gastrulation in the sand dollar Scaphechinus mirabilis are quite different from those in regular echinoids. In this study, we explored the cellular basis of gastrulation in this species with several methods. Cell-tracing experiments revealed that the prospective endodermal cells were convoluted throughout the invagination processes. Histological observation showed that the ectodermal layer remained thickened, and the vegetal cells retained an elongated shape until the last step of invagination. Further, most of the vegetal ectodermal cells were skewed or distorted. Wedge-shaped cells were common in the vegetal ectoderm, especially at the subequatorial region. In these embryos, unlike the embryos of regular echinoids, secondary mesenchyme cells did not seem to exert the force to pull up the archenteron toward the inner surface of the apical plate. In fact, the archenteron cells were not stretched along the axis of elongation and were in close contact with each other. Here we found that gastrulation was completely blocked when the embryos were attached to a glass dish coated with poly-L-lysine, in which the movement of the ectodermal layer was inhibited. These results suggest that a force generated by the thickened ectoderm, rather than rearrangement of the archenteron cells, may play a key role in the archenteron elongation in S. mirabilis embryos.

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PubMed1997

JAGGED2: a putative Notch ligand expressed in the apical ectodermal ridge and in sites of epithelial-mesenchymal interactions.

The Drosophila Notch gene and its ligands, Delta and Serrate, are involved in cell fate determination in a variety of developing tissues. Recently, several Notch, Delta and Serrate homologues have been identified in vertebrates. We report here the cloning of the human and murine JAGGED2 (JAG2), a Serrate-like gene, and the analysis of its expression pattern during embryogenesis. Jag2 was found to be expressed as early as E9 in the surface ectoderm of the branchial arches and in the apical ectodermal ridge (AER) of the developing limb. At E12.5, Jag2 expression is upregulated in differentiated neurons of the central and peripheral nervous system and in the inner neuroblastic layer of the developing retina. Outside the nervous system, Jag2 is expressed in the developing vibrissae follicles, tooth buds, thymus, submandibular gland and stomach. Our findings suggest the involvement of Jagged2 in the development of the mammalian limb, branchial arches, central and peripheral nervous systems and several tissues whose development depends upon epithelial-mesenchymal interactions.

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PubMed2004

Evolutionarily conserved expression pattern and trans-regulating activity of Xenopus p51/p63.

p51/p63, a member of the p53 gene family, is structurally conserved among a wide range of organisms, although the transactivator (TA) and N-terminally truncated (deltaN) isotype producing property seems to vary. Since p51/p63 is thought to play important roles in skin, limb, and craniofacial development in mammals, we examined Xenopus laevis larval and adult tissues for expression of p51/p63. Temporal analyses indicated enhanced transcription of the deltaN form of p51/p63 in premetamorphosis phase (at stage 44-48). p51/p63-positive cells in the inner layer of larval skin expanded to the suprabasal layers during the stratification. The epithelium of limb buds and the maxillofacial ectodermal tissues in tadpoles had a high level expression of p51/p63. The cloned deltaN-A/gamma type Xenopus p51/p63 exhibited a dominant-negative activity against the human TA-A/gamma isotype in a reporter assay. These results suggest that tissue-specific p51/p63-inducing mechanism and isotype-specific transcriptional regulator activities of p51/p63 are conserved between mammals and frogs.

Animals↗
PubMed2005

FGF8 initiates inner ear induction in chick and mouse.

In both chick and mouse, the otic placode, the rudiment of the inner ear, is induced by at least two signals, one from the cephalic paraxial mesoderm and the other from the neural ectoderm. In chick, the mesodermal signal, FGF19, induces neural ectoderm to express additional signals, including WNT8c and FGF3, resulting in induction of the otic placode. In mouse, mesodermal Fgf10 acting redundantly with neural Fgf3 is required for induction of the placode. To determine how the mesodermal inducers of the otic placode are localized, we took advantage of the unique strengths of the two model organisms. We show that endoderm is necessary for otic induction in the chick and that Fgf8, expressed in the chick endoderm subjacent to Fgf19, is both sufficient and necessary for the expression of Fgf19 in the mesoderm. In the mouse, Fgf8 is also expressed in endoderm as well as in other germ layers in the periotic placode region. We show that otic induction fails in embryos null for Fgf3 and hypomorphic for Fgf8 and expression of mesodermal Fgf10 is reduced. Thus, Fgf8 plays a critical upstream role in an FGF signaling cascade required for otic induction in chick and mouse.

Animals↗
PubMed2004

Early stages of test formation in larva of Ascidia malaca (Tunicata, Ascidiacea): ultrastructural and cytochemical investigations.

The swimming larvae of ascidians are entirely covered by a hyalin coat called tunic, or test. This covering consists of two cuticular layers, C1 and C2, which surround an inner compartment composed of an amorphous hyalin matrix with numerous fibrils dispersed inside. Data from the literature agree on the key role played by the cells of the larval ectodermic layer in the synthesis and secretion of larval test components. In the present article are reported ultrastructural and cytochemical investigations made during test formation in the swimming larva of Ascidia malaca. Besides confirming the role played by ectodermic cells during the early stages of test formation, the investigations highlight the way in which the fibrillar component of the test is synthetized and secreted. At the ultrastructural level it has been evidenced that the C1 and C2 cuticular layers originate from the tight packing of fibrils. Based on the data reported in the present study, it is hypothesized that while a relevant part of the fibrils, once secreted, remains dispersed inside the matrix of the inner compartment of the test, quite likely in order to increase its consistency, packing of the remaining fibrils leads to the formation of the C1 and C2 cuticular layers. Packing of the fibrils in C1 and C2 could be favoured by their chemically adhesive nature. This hypothesis is strongly supported by the herewith reported results of the cytochemical investigations carried out on the test of the swimming larva of A. malaca. The cytochemical PA-TCH-SP reaction has in fact evidenced that both fibril types, i.e. those dispersed inside the inner compartment and those packed in the C1 and C2 cuticular layers, are constituted by glycoproteins and/or proteoglycans substances whose adhesive properties are well documented in the literature.

Animals↗
PubMed1995

Limb deformity proteins during avian neurulation and sense organ development.

The nuclear Limb deformity (Ld) proteins (formins) are expressed during the avian primitive streak stages. Initially, they are detected predominantly in cells of the forming notochord, scattered mesodermal precursors and the induced neural plate. No expression is detected in endodermal cells. The subsequent graded distribution of Ld positive cells along the anterior-posterior axis of the neural tube follows the antero-posterior progression of its differentiation. The Ld proteins are also differentially expressed during induction and development of both the inner ear and eye. An unequal distribution of Ld proteins along the dorso-ventral axis of the otic vesicle is observed during its initial patterning. In the eye, the Ld proteins are expressed by the optic vesicle during secondary induction of the lens placode. Following induction, the proteins are also expressed by the newly formed lens placode, a process which is reminiscent of homeogenetic induction. During differentiation of the retina and lens, the Ld domains seem to demarcate territories, giving rise to specific eye structures. A comparative analysis of the Ld distribution and BrdU incorporation in the two sense organs indicates that the proteins are predominantly expressed by committed and/or differentiating (post-mitotic) cells. In general, expression of Ld proteins is induced during determination and remains during differentiation of particular cell-types. This study implies that the nuclear Ld proteins are involved in morphogenesis of both neuro-ectodermal and mesodermal structures.

Animals↗
PubMed1991

Immunohistochemical localization of TGF beta 1, TGF beta 2, and TGF beta 3 in the mouse embryo: expression patterns suggest multiple roles during embryonic development.

Isoform-specific antibodies to TGF beta 1, TGF beta 2, and TGF beta 3 proteins were generated and have been used to examine the expression of these factors in the developing mouse embryo from 12.5-18.5 d post coitum (d.p.c.). These studies demonstrate the initial characterization of both TGF beta 2 and beta 3 in mammalian embryogenesis and are compared with TGF beta 1. Expression of one or all three TGF beta proteins was observed in many tissues, e.g., cartilage, bone, teeth, muscle, heart, blood vessels, lung, kidney, gut, liver, eye, ear, skin, and nervous tissue. Furthermore, all three TGF beta proteins demonstrated discrete cell-specific patterns of expression at various stages of development and the wide variety of tissues expressing TGF beta proteins represent all three primary embryonic germ layers. For example, specific localization of TGF beta 1 was observed in the lens fibers of the eye (ectoderm), TGF beta 2 in the cortex of the adrenal gland (mesoderm), and TGF beta 3 in the cochlear epithelium of the inner ear (endoderm). Compared to the expression of TGF beta mRNA transcripts in a given embryonic tissue, TGF beta proteins were frequently colocalized within the same cell type as the mRNA, but in some cases were observed to localize to different cells than the mRNA, thereby indicating that a complex pattern of transcription, translation, and secretion for TGF beta s 1-3 exists in the mouse embryo. This also indicates that TGF beta 1, beta 2, and beta 3 act through both paracrine and autocrine mechanisms during mammalian embryogenesis.

Animals↗
PubMed2006

Derivation and culture of mouse trophoblast stem cells in vitro.

In the mouse preimplantation embryo, the first cell fate determination segregates two morphologically and functionally distinct cell lineages. One is the inner cell mass, and the other is the trophectoderm. A subset of the trophectoderm maintains a proliferative capacity and forms the extraembryonic ectoderm, the ectoplacental cone, and the secondary giant cells of the early conceptus after implantation. A stem cell population of the trophectoderm lineage can be isolated and maintained in vitro under the presence of fibroblast growth factor 4, heparin, and a feeder layer of mouse embryonic fibroblast cells. Such apparently immortal stem cells, trophoblast stem (TS) cells, exhibit the potential to differentiate to multiple cell types in vitro. TS cells also have the ability to contribute to normal development in chimeras. However, TS cells exclusively contribute to the trophoblastic component of the placenta and of the parietal yolk sac, making a striking contrast with embryonic stem cells, which never contribute to these tissues in chimeras. In this chapter, detailed protocols for the isolation and establishment of TS cell lines from blastocysts and their maintenance are described.

Animals↗
PubMed2004

Modulation of activin/bone morphogenetic protein signaling by follistatin is required for the morphogenesis of mouse molar teeth.

Teeth form as ectodermal appendages, and their morphogenesis is regulated by conserved signaling pathways. The shape of the tooth crown results from growth and folding of inner dental epithelium, and the cusp patterning is regulated by transient signaling centers, the enamel knots. Several signal proteins in the transforming growth factor-beta (TGF beta) superfamily are required for tooth development. Follistatin is an extracellular inhibitor of TGF beta signaling. To investigate the roles of follistatin during tooth development, we analyzed in detail the expression patterns of follistatin, activin beta A, as well as Bmp2, Bmp4, and Bmp7 during tooth morphogenesis. We also examined the tooth phenotypes of follistatin knockout mice and of transgenic mice overexpressing follistatin in the epithelium under the keratin 14 (K14) promoter. The folding of the dental epithelium was aberrant in the molars of follistatin knockout mice, and the cusps were shallow with reduced cell proliferation and lack of anteroposterior polarization. The functions of both primary and secondary enamel knots were apparently disturbed. In K14-follistatin transgenic mice, the molar cusp pattern was also seriously affected (although different from the follistatin knockouts) and the occlusal surfaces of the molars were whorled. Their enamel was prematurely worn. In addition, all of the third molars were missing. Our results indicate that follistatin regulates morphogenesis and shaping of the tooth crown. We propose that finely tuned antagonistic effects between follistatin and TGF beta superfamily signals are critical for enamel knot formation and function, as well as for patterning of tooth cusps.

Activins↗
PubMed1985

RNAs containing B2 repeated sequences are transcribed in the early stages of mouse embryogenesis.

An in situ hybridization technique was used to detect RNAs containing B2 sequences in the early mouse embryo. Accumulation of B2 sequences occurs early from the one cell stage. The level of B2 RNA decreases in the late two cell embryo, and then increases at the moment of second cleavage. In the blastocyst, inner cell mass cells contain more B2 transcripts than trophectoderm cells. In 7.5-day embryos the expression of B2 sequences is restricted to ectoderm and mesoderm. At all stages, transcription of the B2+ strand is greater than B2- strand. We detected B2+ RNAs in the nucleus and cytoplasm, whereas B2- RNAs were present only in the nucleus.

Animals↗
PubMed1985

Clonal analysis of early mammalian development.

Various extrinsic markers have been used to label single cells in the early mouse embryo. However, they are appropriate only for short-term experiments because of their susceptibility to dilution. Studies on cell lineage and commitments have therefore depended mainly on exploiting genes as markers by combining cells from embryos that differ in genotype at particular loci. Tissue recombination and transplantation experiments using such indelible intrinsic markers have enabled the fate of different cell populations in the blastocyst to be determined with reasonable precision. The trophectoderm and inner cell mass (i.c.m.) give rise to distinct complementary groups of tissues in the later conceptus, as do the primitive endodermal and primitive ectodermal components of the more mature i.c.m. When cloned by blastocyst injection, single i.c.m. cells colonize only those parts of host conceptuses that are derived from their tissue of origin. Thus, while clonal descendants of early i.c.m. cells can contribute to all tissues other than those of trophectodermal origin, primitive endodermal and primitive ectodermal clones are restricted, respectively, to the extraembryonic endoderm versus all i.c.m. derivatives except the extraembryonic endoderm. Interestingly, individual primitive ectoderm cells can include both germ cells and somatic cells among their mitotic descendants. By using the genetically determined presence versus absence of cytoplasmic malic enzyme activity as a cell marker, the deployment of clones has been made visible in situ in whole-mount preparations of extraembryonic membranes. Very little mixing of donor and host cells was seen in either the endoderm of the visceral yolk sac or the mesodermal and ectodermal layers of the amnion. In contrast, mosaicism in the parietal endoderm was so fine grained that, in all except 1 of 15 fields from several specimens that were analysed, the arrangement of donor and host cells did not differ significantly from that expected on the basis of their random association.

Amnion↗
PubMed1998

The development of the vertebrate inner ear.

The inner ear is a complex sensory organ responsible for balance and sound detection in vertebrates. It originates from a transient embryonic structure, the otic vesicle, that contains all of the information to develop autonomously into the mature inner ear. We review here the development of the otic vesicle, bringing together classical embryological experiments and recent genetic and molecular data. The specification of the prospective ectoderm and its commitment to the otic fate are very early events and can be related to the expression of genes with restricted expression domains. A combinatorial gene expression model for placode specification and diversification, based on classical embryological evidence and gene expression patterns, is discussed. The formation of the otic vesicle is dependent on inducing signals from endoderm, mesoderm and neuroectoderm. Ear induction consists of a sequence of discrete instructions from those tissues that confer its final identity on the otic field, rather than a single all-or-none process. The important role of the neural tube in otic development is highlighted by the abnormalities observed in mouse mutants for the Hoxa1, kreisler and fgf3 genes and those reported in retinoic acid-deficient quails. Still, the nature of the relation between the neural tube and otic development remains unclear. Gene targeting experiments in the mouse have provided evidence for genes potentially involved in regional and cell-fate specification in the inner ear. The disruption of the mouse Brn3.1 gene identifies the first mutation affecting sensory hair-cell specification, and mutants for Pax2 and Nkx5.1 genes show their requirement for the development of specific regions of the otic vesicle. Several growth-factors contribute to the patterned cell proliferation of the otic vesicle. Among these, IGF-I and FGF-2 are expressed in the otic vesicle and may act in an autocrine manner. Finally, little is known about early mechanisms involved in guiding ear innervation. However, targeted disruption of genes coding for neurotrophins and Trk receptors have shown that once synaptic contacts are established, they depend on specific trophic interactions that involve these two gene families. The accessibility of new cellular and molecular approaches are opening new perspectives in vertebrate development and are also starting to be applied to ear development. This will allow this classical and attractive model system to see a rapid progress in the near future.

Animals↗
PubMed2000

Molecular genetics of pattern formation in the inner ear: do compartment boundaries play a role?

The membranous labyrinth of the inner ear establishes a precise geometrical topology so that it may subserve the functions of hearing and balance. How this geometry arises from a simple ectodermal placode is under active investigation. The placode invaginates to form the otic cup, which deepens before pinching off to form the otic vesicle. By the vesicle stage many genes expressed in the developing ear have assumed broad, asymmetrical expression domains. We have been exploring the possibility that these domains may reflect developmental compartments that are instrumental in specifying the location and identity of different parts of the ear. The boundaries between compartments are proposed to be the site of inductive interactions required for this specification. Our work has shown that sensory organs and the endolymphatic duct each arise near the boundaries of broader gene expression domains, lending support to this idea. A further prediction of the model, that the compartment boundaries will also represent lineage-restriction compartments, is supported in part by fate mapping the otic cup. Our data suggest that two lineage-restriction boundaries intersect at the dorsal pole of the otocyst, a convergence that may be critical for the specification of endolymphatic duct outgrowth. We speculate that the patterning information necessary to establish these two orthogonal boundaries may emanate, in part, from the hindbrain. The compartment boundary model of ear development now needs to be tested through a variety of experimental perturbations, such as the removal of boundaries, the generation of ectopic boundaries, and/or changes in compartment identity.

Animals↗
PubMed1982

Preferential paternal X inactivation in extraembryonic tissues of early mouse embryos.

The preferential expression of the maternal X chromosome seen in certain extraembryonic membranes of the mouse was studied by investigating the tissues from which these membranes are derived during early development. The electrophoretic variant of the X-coded enzyme PGK-1 (phosphoglycerate kinase) was used to distinguish the expression of the maternal from the paternal X chromosome in heterozygous females. Both the extraembryonic ectoderm and primary endoderm of 6 1/2-day female egg cylinders gave almost exclusive expression of the maternal form of the enzyme whereas the epiblast gave near equal expression of the two parental alleles. No paternal PGK-1 band could be detected in samples of pooled 3 1/2-day blastocysts, but after 3 or 4 days of culture in vitro a faint paternal band was seen in the resultant outgrowths. The activity of the maternal band in these latter samples had increased greatly from that of the blastocysts, consistent with preferential expression of the maternal Pgk-1 allele in the trophoblastic cells of the outgrowths, while both alleles are expressed in inner-cell-mass cells. The results strongly support the idea that non-random X-chromosome expression is due to preferential paternal X inactivation in trophectoderm (from which extraembryonic ectoderm is derived) and in primary endoderm, and not to cell selection.

Animals↗