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PubMed1997

Mesodermal defects and cranial neural crest apoptosis in alpha5 integrin-null embryos.

Alpha5beta1 integrin is a cell surface receptor that mediates cell-extracellular matrix adhesions by interacting with fibronectin. Alpha5 subunit-deficient mice die early in gestation and display mesodermal defects; most notably, embryos have a truncated posterior and fail to produce posterior somites. In this study, we report on the in vivo effects of the alpha5-null mutation on cell proliferation and survival, and on mesodermal development. We found no significant differences in the numbers of apoptotic cells or in cell proliferation in the mesoderm of alpha5-null embryos compared to wild-type controls. These results suggest that changes in overall cell death or cell proliferation rates are unlikely to be responsible for the mesodermal deficits seen in the alpha5-null embryos. No increases in cell death were seen in alpha5-null embryonic yolk sac, amnion and allantois compared with wild-type, indicating that the mutant phenotype is not due to changes in apoptosis rates in these extraembryonic tissues. Increased numbers of dying cells were, however, seen in migrating cranial neural crest cells of the hyoid arch and in endodermal cells surrounding the omphalomesenteric artery in alpha5-null embryos, indicating that these subpopulations of cells are dependent on alpha5 integrin function for their survival. Mesodermal markers mox-1, Notch-1, Brachyury (T) and Sonic hedgehog (Shh) were expressed in the mutant embryos in a regionally appropriate fashion. Both T and Shh, however, showed discontinuous expression in the notochords of alpha5-null embryos due to (1) degeneration of the notochordal tissue structure, and (2) non-maintenance of gene expression. Consistent with the disorganization of notochordal signals in the alpha5-null embryos, reduced Pax-1 expression and misexpression of Pax-3 were observed. Anteriorly expressed HoxB genes were expressed normally in the alpha5-null embryos. However, expression of the posteriormost HoxB gene, Hoxb-9, was reduced in alpha5-null embryos. These results suggest that alpha5beta1-fibronectin interactions are not essential for the initial commitment of mesodermal cells, but are crucial for maintenance of mesodermal derivatives during postgastrulation stages and also for the survival of some neural crest cells.

Animals↗
PubMed1997

The allocation of epiblast cells to the embryonic heart and other mesodermal lineages: the role of ingression and tissue movement during gastrulation.

The cardiogenic potency of cells in the epiblast of the early primitive-streak stage (early PS) embryo was tested by heterotopic transplantation. The results of this study show that cells in the anterior and posterior epiblast of the early PS-stage embryos have similar cardiogenic potency, and that they differentiated to heart cells after they were transplanted directly to the heart field of the late PS embryo. That the epiblast cells can acquire a cardiac fate without any prior act of ingression through the primitive streak or movement within the mesoderm suggests that neither morphogenetic event is critical for the specification of the cardiogenic fate. The mesodermal cells that have recently ingressed through the primitive streak can express a broad cell fate that is characteristic of the pre-ingressed cells in the host when they were returned to the epiblast. However, mesoderm cells that have ingressed through the primitive streak did not contribute to the lateral plate mesoderm after transplantation back to the epiblast, implying that some restriction of lineage potency may have occurred during ingression. Early PS stage epiblast cells that were transplanted to the epiblast of the mid PS host embryos colonised the embryonic mesoderm but not the extraembryonic mesoderm. This departure from the normal cell fate indicates that the allocation of epiblast cells to the mesodermal lineages is dependent on the timing of their recruitment to the primitive streak and the morphogenetic options that are available to the ingressing cells at that instance.

Animals↗
PubMed2000

Wingless effects mesoderm patterning and ectoderm segmentation events via induction of its downstream target sloppy paired.

Inactivation of either the secreted protein Wingless (Wg) or the forkhead domain transcription factor Sloppy Paired (Slp) has been shown to produce similar effects in the developing Drosophila embryo. In the ectoderm, both gene products are required for the formation of the segmental portions marked by naked cuticle. In the mesoderm, Wg and Slp activities are crucial for the suppression of bagpipe (bap), and hence visceral mesoderm formation, and the promotion of somatic muscle and heart formation within the anterior portion of each parasegment. In this report, we show that, during these developmental processes, wg and slp act in a common pathway in which slp serves as a direct target of Wg signals that mediates Wg effects in both germ layers. We present evidence that the induction of slp by Wg involves binding of the Wg effector Pangolin (Drosophila Lef-1/TCF) to multiple binding sites within a Wg-responsive enhancer that is located in 5' flanking regions of the slp1 gene. Based upon our genetic and molecular analysis, we conclude that Wg signaling induces striped expression of Slp in the mesoderm. Mesodermal Slp is then sufficient to abrogate the induction of bagpipe by Dpp/Tinman, which explains the periodic arrangement of trunk visceral mesoderm primordia in wild type embryos. Conversely, mesodermal Slp is positively required, although not sufficient, for the specification of somatic muscle and heart progenitors. We propose that Wg-induced slp provides striped mesodermal domains with the competence to respond to subsequent slp-independent Wg signals that induce somatic muscle and heart progenitors. We also propose that in wg-expressing ectodermal cells, slp is an integral component in an autocrine feedback loop of Wg signaling.

Animals↗
PubMed1987

A mesoderm-inducing factor is produced by Xenopus cell line.

Inductive interactions play a major role in the diversification of cell types during vertebrate development. These interactions have been extensively studied in amphibian embryos (usually Xenopus laevis) where the earliest is mesoderm induction, in which an equatorial mesodermal rudiment is induced from the animal hemisphere under the influence of signal from the vegetal hemisphere. The molecular basis of mesoderm induction is unknown, although Tiedemann has isolated a protein form 9- to 13-day chick embryos that has the properties one would expect of a mesoderm-inducing factor. However, the relevance of this molecule to the events of early amphibian development is unclear, and it is a matter of some importance to discover a Xenopus mesoderm-inducing factor. In this paper I show that the Xenopus XTC cell line secretes mesoderm-inducing activity into the culture medium. Isolated animal pole regions cultured in XTC-conditioned medium differentiate into muscle and notochord, while controls form 'atypical epidermis'. Three different cell lines -XL, XL177 and KR- secrete no such activity indicates that the active principle is heat stable, trypsin sensitive, nondialysable, and has an apparent relative molecular mass of about 16,000. Work is in progress to characterize the activity further and to discover whether the mesoderm-inducing factor is also present in normal embryos.

Activins↗
PubMed2001

Fox (forkhead) genes are involved in the dorso-ventral patterning of the Xenopus mesoderm.

Fox (forkhead/winged helix) genes encode a family of transcription factors that are involved in embryonic pattern formation, regulation of tissue specific gene expression and tumorigenesis. Several of them are transcribed during Xenopus embryogenesis and are important for the patterning of ectoderm, mesoderm and endoderm. We have isolated three forkhead genes that are activated during gastrulation and play an important role in the dorso-ventral patterning of the mesoderm. XFKH1 (FoxA4b), the first vertebrate forkhead gene to be implicated in embryonic pattern formation, is expressed in the Spemann-Mangold organizer region and later in the embryonic notochord. XFKH7, the Xenopus orthologue of the murine Mfh1(Foxc2), is expressed in the presomitic mesoderm, but not in the notochord or lateral plate mesoderm. Finally, XFD-13'(FoxF1b)1 is expressed in the lateral plate mesoderm, but not in the notochord or presomitic mesoderm. Expression pattern and functional experiments indicate that these three forkhead genes are involved in the dorso-ventral patterning of the mesoderm.

Amino Acid Sequence↗
PubMed1992

Mesoderm-inducing factors and the control of gastrulation.

One of the reasons that we know so little about the control of vertebrate gastrulation is that there are very few systems available in which the process can be studied in vitro. In this paper, we suggest that one suitable system might be provided by the use of mesoderm-inducing factors. In amphibian embryos such as Xenopus laevis, gastrulation is driven by cells of the mesoderm, and the mesoderm itself arises through an inductive interaction in which cells of the vegetal hemisphere of the embryo emit a signal which acts on overlying equatorial cells. Several factors have recently been discovered that modify the pattern of mesodermal differentiation or induce mesoderm from presumptive ectoderm. Some of these mesoderm-inducing factors will also elicit gastrulation movements, which provides a powerful model system for the study of gastrulation, because a population of cells that would not normally undertake the process can be induced to do so. In this paper, we use mesoderm-inducing factors to attempt to answer four questions. How do cells know when to gastrulate? How do cells know what kind of gastrulation movement to undertake? What is the cellular basis of gastrulation? What is the molecular basis of gastrulation?

Activins↗
PubMed1978

[Reciprocal homology of the preotic mesodermal segments of representatives of different classes of vertebrates].

The data of the literature and those of the author on the origin of preotic mesodermal segments are discussed. Only in Cyclostomata all preotic segments are formed from the wall of archenteron and are larval segments. In all the gnathos tomata, the primary gastral segments are substituted, to different degrees, by postlarval peristonal mesoderm. The preotic mesomeres of Cyclostomata are homologous to II--IV mesomeres of Branchiostoma lanceolata. The anterior cephalic cavity and the premandibular segment of the elasmobranchia are homologous to I and II segments of Branchiostoma lanceolata. The mandibular mesoderm of the elasmobranchia includes the gastral mesoderm (homologous to III and some subsequent segments of Brachiostoma lanceolata) and peristomal mesoderm. The mandibular mesoderm in higher vertebrates has the same composition, but their anterior larval segments disappear and are substituted by gastral part of the mandibular mesoderm.

Amphibians↗
PubMed1977

Mesodermal expansion after arrest of the edge in the area vasculosa of the chick.

To investigate whether mesodermal expansion in the area vasculosa is caused by tension produced by outward migration of cells either in the somatic mesoderm or at the mesodermal edge on an ectodermal substratum, stage 18--20 embryos were transferred to a culture dish. There mesodermal expansion proximal to an arrested edge could be compared with that proximal to a moving edge by measuring the amount of vascular elongation occurring in each. A proximo-distal gradient in vascular elongation rate was detected both in normal embryos in ovo and in explants. This gradient was reversed following arrest of the edge, and the rate of vascular elongation proximal to the arrested edge decreased to 60--70% of that proximal to a moving edge. Nearly all of the mesoderm producing this expansion was located in the proximal two-thirds of the area vasculosa, where vascular elongation rate on the stopped side of the explant was not significantly different from that on the moving side. Similar results were obtained in the absence of the ectoderm, and when liquid culture medium was used instead of semisolid medium. It is concluded that tensile force derived from mesodermal migration plays no role in expansion of the proximal two-thirds of the area vasculosa mesoderm.

Animals↗
PubMed1976

Mixed mesodermal tumor of the uterine body: relationship between histology and survival.

A clinico-pathological study of 20 cases of mixed mesodermal tumor of the uterine body is reported. Fifteen tumors were found after menopause. The mean age of all cases was 55.5 years. Histologically, mixed mesodermal tumors consisted of two different components; epithelial and sarcomatous patterns, in 18 cases. Mixed mesodermal tumors in four of the 18 cases had no adenocarcinomatous elements but showed a benign glandular structure. In the remaining two tumors, epithelial patterns were absent and only heterologous sarcomatous elements were found. Ten of the patients had received hysterectomy more than five years ago. Three of these patients, having no malignant but benign epithelial component, showed a relatively good prognosis. Adenocarcinomatous elements were found in six cases, and four patients with carcinomatous elements had poor prognosis. It can be stated that the prognosis of mixed mesodermal tumor chiefly depends on the malignancy of epithelial components, when comparing the prognosis of the tumors at the same clinical stage. On the other hand, sarcomatous elements are not likely to reflect the prognosis of the tumors. Mixed mesodermal tumor is monodermal in origin, namely, mesodermal origin, and might arise from the Muellerian duct or more primitive mesodermal tissue.

Adult↗
PubMed1998

Dual role for the zeste-white3/shaggy-encoded kinase in mesoderm and heart development of Drosophila.

A Drosophila homolog of the serine/threonine kinase GSK-3 beta, encoded by the zest-white3/shaggy gene (zw3), has been implicated as a maternally provided antagonist of zygotic signaling by the secreted segmentation gene wingless (wg). The wg signal apparently causes a spatially localized inhibition of the ubiquitous repressor function of zw3. This double negative mechanism of signal transduction has been shown to mediate the patterning function of Wg in a number of developmental processes. Although wg is absolutely required for specifying the heart progenitors within the mesoderm of Drosophila, the role of zw3 in this process has been unclear. Here, we present evidence that zw3 has a dual role in mesoderm development: (1) zw3 acts as an antagonist in cardiogenic wg signal transduction, and (2) zw3 also seems to be required to promote positively the formation of a larger mesodermal region, the tinman- and dpp-dependent "dorsal mesoderm," which is a prerequisite not only for cardiogenesis, but also for visceral mesoderm formation. We also demonstrate that a recently identified proximal component of the wg cascade, which is a transcription factor encoded by pangolin/dTCF (dTCF), also seems to mediate wg-dependent cardiogenesis. Further, we present evidence that Notch (N), which opposes wg signaling in other situations, is unlikely to be directly involved in the cardiogenic wg pathway, but seems to have multiple other myogenic functions, one of which is to inhibit mesoderm differentiation altogether, when overexpressed as a constitutively active form.

Animals↗
PubMed1993

Evidence that the border of the neural plate may be positioned by the interaction between signals that induce ventral and dorsal mesoderm.

In the early Xenopus embryo, a quadrant of endodermal cells that have descended from the vegetal dorsal localization in the zygote produces signals that pass into the animal hemisphere and induce dorsal mesoderm from the marginal zone. From the remaining three quadrants of the bordering endoderm, signals pass into the animal hemisphere and induce ventral mesoderm in the marginal region. There is evidence that suggests that these same mesoderm-inducing signals continue through the plane of the tissue of the animal hemisphere where they may at least begin the processes of neural and epidermal induction by changing the competence of the prospective ectodermal cells, and possibly influencing the early regional biasing of later expression of at least some gene products, such as Epi-1 whose expression in the future epidermal domain seems specified before gastrulation. We hypothesized that the interaction of the ventral and dorsal signals within the plane of the tissue of the animal hemisphere may position the border of the neural plate. If this is so, then transplantation into the animal pole of cells that signal induction of ventral mesoderm should drive the neural plate boundary back toward the blastopore and shorten the anterior-posterior axis. Removal of cells that induce ventral mesoderm should result in an axis that is longer than normal. Results of our experiments support these predictions. Also, by late pregastrula stage 9, increasing the ventral signals has no effect. Thus the evidence suggests that the position of the anterior neural plate boundary is established before gastrulation begins by the interaction of the signals that induce the ventral and dorsal mesoderm.

Animals↗
PubMed1989

Transfer of dorsoventral information from mesoderm to ectoderm at the onset of limb development.

Control of dorsoventral patterns in the chick at the prelimb stages resides in the limb mesoderm. Recombination experiments at stage 14, with dorsoventrally reversed ectoderm, result in wings with mesodermal dorsoventral polarity. Similar recombinations at stage 16 show that the ectoderm has acquired dorsoventral information and can impose this polarity on the patterns of mesodermal differentiation in the distal regions of the wing. The dorsoventral information in the ectoderm comes from the mesoderm, which transfers this information to the overlying ectoderm between stages 14 and 16. The initial dorsoventral overlying ectoderm between stages 14 and 16. The initial dorsoventral information in the ectoderm is not stable and can be reprogrammed by stage 14 mesoderm. Subsequently, there is a gradual stabilization of the ectodermal information. At the same time the mesoderm loses its capacity to reprogram dorsoventral information in the ectoderm.

Animals↗
PubMed1993

Secretion and mesoderm-inducing activity of the TGF-beta-related domain of Xenopus Vg1.

Vg1 is a maternal mRNA localized to the vegetal hemisphere of Xenopus embryos during blastula stages, a region responsible for the induction of mesoderm in the adjacent marginal zone. Its homology to the transforming growth factor-beta family, which includes several proteins with mesoderm-inducing activity, suggests a role for Vg1 as an endogenous mesoderm-inducing factor. However, expression of Vg1 protein in the animal hemisphere, following injection of synthetic mRNA, has no effect on development, and isolated animal caps are not mesodermalized. It is shown that Vg1 protein fails to form dimers and is not processed to release the putative bioactive domain. Furthermore it is shown that the N-terminal signal peptide of Vg1 is not cleaved following translocation into the ER, which may explain the failure of this protein to dimerize. To explore the role of Vg1 in amphibian development, a fusion protein has been made of the preproregion of Xenopus bone morphogenetic protein-4 and the putative bioactive C-terminal domain of Vg1. This fusion protein forms dimers and the C-terminal domain of Vg1 is secreted. Injection of this construct into Xenopus embryos induces the formation of a second dorsal axis and isolated animal caps are mesodermalized. The results are consistent with a role for Vg1 in mesoderm induction during Xenopus development.

Amino Acid Sequence↗
PubMed1994

Specification of mesodermal pattern in Xenopus laevis by interactions between Brachyury, noggin and Xwnt-8.

We demonstrate that the nuclear, sequence-specific DNA-binding protein Xbra causes dorsal mesodermal differentiation of animal cap ectoderm when co-expressed with the secreted proteins noggin and Xwnt-8. None of these molecules causes dorsal mesoderm formation when expressed alone. Co-expression of Xenopus Brachyury (Xbra) mRNA with noggin mRNA in animal caps specifies the main dorsal tissues, namely muscle, notochord and neural tissue. Co-expression of Xbra with Xwnt-8, in contrast, converts animal caps to muscle masses. We have previously shown that expression of Xbra alone in animal caps is sufficient to specify ventral mesoderm which expresses Xhox3 and low levels of muscle-specific actin. We now conclude that the putative transcription factor Xbra defines a cell state in the vertebrate embryo which can respond to diffusible dorsal signals such as noggin and Xwnt-8, resulting in dorsal mesodermal differentiation. In the absence of such dorsal signals Xbra causes ventral mesodermal differentiation. This state is only partially maintained after the mid-blastula transition as it permits the dorsal response to zygotically expressed noggin but it does not allow a dorsal response to zygotically expressed Xwnt-8, which elicits only ventral mesodermal differentiation.

Animals↗
PubMed1995

Identification of a potential regulator of early transcriptional responses to mesoderm inducers in the frog embryo.

The activin/transforming growth factor-beta (TGF-beta) family of peptide growth factors plays a central role in the induction of mesoderm during early Xenopus embryogenesis. Immediate transcriptional responses to mesoderm-inducing signals have been described, but the signal transduction steps leading to these early responses are unknown. We describe here the first pre-transcriptional response to activin/TGF-beta mesoderm inducers in the early embryo. We have identified a cellular factor which binds to a 50 bp portion of the promoter for an activin/TGF-beta early response gene. This factor is activated within 4 min of treatment of embryonic prospective ectoderm with mesoderm-inducing factors, making it the earliest response to these factors described in early embryos. This factor can be activated throughout early cleavage and blastula stages, is activated by mesoderm inducers of the activin/TGF-beta superfamily but not the fibroblast growth factor (FGF) family, and does not appear to require an endogenous FGF signal for activation. Characterization of this factor provides a powerful tool for studying the early steps in the induction of mesoderm by members of the activin/TGF-beta superfamily.

Activins↗
PubMed1983

The culture of chick embryo mesoderm cells in hydrated collagen gels.

Chick embryo mesoderm cells are various stages of differentiation were cultured in three-dimensional matrices of hydrated collagen. The tissues used were: stage 5 mesoderm from regions adjacent to the primitive streak; stage 12 mesoderm, comprising somitic, unsegmented (segmental plate) and lateral plate mesoderm; and stage 18 sclerotome. Explants were examined by phase contrast microscopy, including time-lapse, and scanning and transmission electron microscopy. The cells showed an increased ability to adhere to, and move in, the collagen gel with advancing stage. Of the stage 12 tissues, the unsegmented mesoderm was initially the slowest to grow out of the explant. Sclerotome cells showed by far the greatest ability to move within the gel. Where the collagen fibrils were randomly oriented, the cell morphology was polypodial and advancing lamellipodia showed clear undulations at their leading edges. A distinction was drawn between these undulations and the classical major ruffles which are seen in two-dimensional culture to uplift and pass back along the cell surface. The latter were not seen in the collagen matrix and were presumably suppressed by the three-dimensional culture configuration while the leading edge undulations were not. Ultrastructural examination showed that the cells possessed patches of amorphous material on their surface, which was sometimes interposed between the plasma membrane and collagen fibrils. Addition of hyaluronic acid (2 mg/ml) had an effect only the segmented mesoderm, where outgrowth was enhanced. Although the addition of plasma fibronectin (50 micrograms/ml) to the cultures did not affect any of the tissues, the removal of this substance, by antifibronectin antiserum or by the use of fibronectin depleted serum, inhibited outgrowth in most cases. The only tissue not reproducibly inhibited in this way was sclerotome. Alignment of the collagen fibres by the explants was observed, accompanied by an elongation of the outgrowing cells which, in bipolar form, preferentially moved up and down the aligned tracts. Scanning electron microscopy suggested that cell processes attached to, and presumably exerted tension on, bundles of fibrils thereby pulling them into line. Cell-to-cell contact was not accompanied by contact paralysis as judged by time-lapse micrography.

Animals↗
PubMed1993

Reaction-diffusion control of heart development: evidence for activation and inhibition in precardiac mesoderm.

In axolotl embryos homozygous for the cardiac-lethal (c) gene, the heart never begins to beat. Recently, we demonstrated that the c gene affects the heart mesoderm directly, making the latter incapable of responding to normal inductive stimuli. Based on these results, we proposed that a reaction-diffusion mechanism controls the later stages of vertebrate cardiogenesis. In the present study, we use a series of transplantations to examine the precardiac mesoderm of wild-type and cardiac-lethal mutant axolotl embryos for the activation and inhibition predicted by our model. When one or both heart primordia in c/c embryos were replaced with +/+ tissue at early stages, functional hearts developed, indicating that an activator-like activity is present in wild-type heart mesoderm. At later stages, replacement of the entire heart-field mesoderm also rescued mutant embryos, but replacement of only the heart-forming mesoderm did not, indicating that the mutant heart field has inhibitory properties. These results demonstrate that activator- and inhibitor-like factors are present in pre-cardiac mesoderm and thus provide evidence for reaction-diffusion control of postinductive heart development.

Ambystoma↗
PubMed1994

An inhibitory effect of Xenopus gastrula ectoderm on muscle cell differentiation and its role for dorsoventral patterning of mesoderm.

In Amphibia, mesoderm cells such as notochord, muscle, and blood are formed as a result of mesoderm induction, the first known inductive interaction during the embryonic development of Vertebrates. Recent evidence shows, however, that, in addition to mesoderm induction, further cell-cell interactions during gastrulation also play an important role in the differentiation of mesoderm cells in Xenopus embryos. Here we report the existence of an inhibitory effect of gastrula ectoderm on muscle cell differentiation. When placed in contact with a muscle progenitor cell population, ectoderm from the ventral side of a gastrula embryo exerts an inhibitory effect on MyoD expression and muscle differentiation. This inhibitory effect is not observed on notochord differentiation. Dorsal ectoderm shows the same extent of inhibitory effect if it is isolated at the early-gastrula stage but gradually loses its effect during gastrulation as it is induced to become neural tissue. Cell mixing experiments have shown that this inhibitory effect, clearly seen in ventral ectoderm, is not observed in ventral mesoderm cells. We propose that the ectoderm emits a signal counteracting dorsalization and the community effect and that this signal plays an important role in the correct dorsoventral patterning of mesoderm.

Animals↗