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PubMed2005

Mesodermal adenosarcoma of the testis.

Biphasic neoplasms with a benign to atypical epithelial component and a usually low-grade malignant stromal component have been reported in various sites, probably being best known for their occurrence in the uterine corpus (mullerian adenosarcoma). We report a tumor of this type that occurred in the testis of a 76-year-old man and, to our knowledge, is the first mesodermal adenosarcoma reported at this site. The patient had scrotal swelling for many years with a pronounced increase in the swelling over the past 2 years. A large complex solid-cystic testicular tumor was evident on ultrasound, and examination of a radical orchiectomy specimen showed a 6.5-cm mass. On microscopic examination, the neoplasm had a phyllodes-like appearance with bland cuboidal to flattened epithelium covering polypoid fronds, and lining glands and cysts. The stroma varied from cellular, particularly where it condensed around the glands and cysts, to hypocellular and hyalinized. It was immunoreactive for muscle specific actin, CD10, and to a lesser degree, desmin. This case expands the known sites where mesodermal adenosarcoma may occur. The histogenesis is speculative, but possible options are discussed.

Actins↗
PubMed1996

A novel mesoderm inducer, Madr2, functions in the activin signal transduction pathway.

A functional assay to clone mouse mesoderm inducers has identified the mouse gene Mad related 2 (Madr2). Madr2 induces dorsal mesoderm from Xenopus ectoderm and can mimic the organizer in recruiting neighboring cells into a second axis. By analyzing the expression of a lacZ/Madr2 fusion protein, we find Madr2 confined to the nucleus in the deep, anterior cells of the second axis, whereas in epidermal and more posterior cells the protein is cytoplasmically localized. This context-dependent nuclear localization suggests that in certain regions of the embryo, Madr2 responds to a localized signal and amplifies this signal to form the second axis. Furthermore, although Madr2 remains unlocalized in ectodermal explants, addition of activin enhances the concentration of Madr2 in the nucleus. Significantly, a functional lacZ fusion to a carboxy-terminal portion of Madr2 is nuclear localized even in the absence of activin. This indicates that Madr2 contains a domain that can activate downstream components and a repressive domain that anchors the protein in the cytoplasm. Nuclear localization of Madr2 in response to activin, and the activin-like phenotypes induced by overexpression of Madr2, indicate that Madr2 is a signal transduction component that mediates the activity of activin.

Activins↗
PubMed1997

Overexpression of Stra13, a novel retinoic acid-inducible gene of the basic helix-loop-helix family, inhibits mesodermal and promotes neuronal differentiation of P19 cells.

We report the cDNA cloning of Stra13, a novel retinoic acid (RA)-inducible gene from P19 embryonal carcinoma cells that encodes a basic helix-loop-helix (bHLH) protein that shows the highest sequence similarities to the Drosophila Hairy and Enhancer of split and mouse Hes proteins. Stra13 does not bind to the known consensus motifs (E-box and N-box) for bHLH proteins, but can repress activated transcription (through an alpha-helix rich domain) in part by interaction with general factors of the basal transcription machinery. During mouse embryogenesis, Stra13 RNA is expressed in the neuroectoderm, and also in a number of mesodermal and endodermal derivatives. Remarkably, overexpression of Stra13 in P19 cells results in neuronal differentiation in monolayer culture, under conditions where wild-type P19 cells only undergo mesodermal/endodermal differentiation. This neuronal differentiation is accompanied by an altered expression of mesodermal and neuronal markers, indicating that Stra13 could be one of the earliest RA target genes whose expression is required for repression of mesodermal/endodermal differentiation and/or induction of neuronal differentiation when P19 cell aggregates are exposed to RA. Our results raise the possibility that Stra13 could be involved as a repressor in a number of decision events occurring during differentiation of various cell lineages.

Amino Acid Sequence↗
PubMed1997

The winged helix transcription factor MFH1 is required for proliferation and patterning of paraxial mesoderm in the mouse embryo.

The gene mfh1, encoding a winged helix/forkhead domain transcription factor, is expressed in a dynamic pattern in paraxial and presomitic mesoderm and developing somites during mouse embryogenesis. Expression later becomes restricted to condensing mesenchyme of the vertebrae, head, limbs, and kidney. A targeted disruption of the gene was generated by homologous recombination in embryonic stem cells. Most homozygous mfh1 null embryos die prenatally but some survive to birth, with multiple craniofacial and vertebral column defects. Using molecular markers, we show that the initial formation and patterning of somites occurs normally in mutants. Differentiation of sclerotome-derived cells also appears unaffected, although a reduction of the level of some markers [e.g., mtwist, mf1, scleraxis, and alpha1(II) collagen] is seen in the anterior of homozygous mutants. The most significant difference, however, is a marked reduction in the proliferation of sclerotome-derived cells, as judged by BrdU incorporation. This proliferation defect was also seen in micromass cultures of somite-derived cells treated with transforming growth factor beta1 and fibroblast growth factors. Our findings establish a requirement for a winged helix/forkhead domain transcription factor in the development of the paraxial mesoderm. A model is proposed for the role of mfh1 in regulating the proliferation and differentiation of cell lineages giving rise to the axial skeleton and skull.

Animals↗
PubMed2005

Mesodermally expressed Drosophila microRNA-1 is regulated by Twist and is required in muscles during larval growth.

Although hundreds of evolutionarily conserved microRNAs have been discovered, the functions of most remain unknown. Here, we describe the embryonic spatiotemporal expression profile, transcriptional regulation, and loss-of-function phenotype of Drosophila miR-1 (DmiR-1). DmiR-1 RNA is highly expressed throughout the mesoderm of early embryos and subsequently in somatic, visceral, and pharyngeal muscles, and the dorsal vessel. The expression of DmiR-1 is controlled by the Twist and Mef2 transcription factors. DmiR-1KO mutants, generated using ends-in gene targeting, die as small, immobilized second instar larvae with severely deformed musculature. This lethality is rescued when a DmiR-1 transgene is expressed specifically in the mesoderm and muscle. Strikingly, feeding triggers DmiR-1KO-associated paralysis and death; starved first instar DmiR-1KO larvae are essentially normal. Thus, DmiR-1 is not required for the formation or physiological function of the larval musculature, but is required for the dramatic post-mitotic growth of larval muscle.

Animals↗
PubMed2006

The regulation of mesodermal progenitor cell commitment to somitogenesis subdivides the zebrafish body musculature into distinct domains.

The vertebrate musculature is produced from a visually uniform population of mesodermal progenitor cells (MPCs) that progressively bud off somites populating the trunk and tail. How the MPCs are regulated to continuously release cells into the presomitic mesoderm throughout somitogenesis is not understood. Using a genetic approach to study the MPCs, we show that a subset of MPCs are set aside very early in zebrafish development, and programmed to cell-autonomously enter the tail domain beginning with the 16th somite. Moreover, we show that the trunk is subdivided into two domains, and that entry into the anterior trunk, posterior trunk, and tail is regulated by interactions between the Nodal and bone morphogenetic protein (Bmp) pathways. Finally, we show that the tail MPCs are held in a state we previously called the Maturation Zone as they wait for the signal to begin entering somitogenesis.

Animals↗
PubMed1976

The surface charge of mesodermal and neural cells of Triturus embryos.

The electrical surface charge of disaggregated mesodermal and neural cells of the neurula stage of Triturus vulgaris embryos is estimated by using the apparatus described in Figure 1. The results showed a significant difference between the net charges of these two cell types: the neural cells had a clearly negative charge, whereas the mesodermal cells seemed to be more or less neutral. The difference of the surface charges may partly explain the "sorting-out" phenomenon in the mixed reaggregates of the disaggregated cells.

Animals↗
PubMed2006

Characterization of myeloid cells derived from the anterior ventral mesoderm in the Xenopus laevis embryo.

A recent study revealed the presence of a unique population of myeloid cells in the anterior ventral (AV) mesoderm of Xenopus laevis embryo, as characterized by the expression of peroxidase 2 (POX2), which encodes for a leukocyte-specific enzyme. The current report further characterized the POX2-positive cells in terms of their contribution to hematopoiesis in tadpole and regulatory mechanism in differentiation. Grafting experiments with cytogenetically labeled tissues revealed that AV-derived mesoderm supplies a transient population of migrating leukocytes in the mesenchyme of early tadpole. These cells were rarely found in blood vessels at any stages. Using a ventral marginal zone explant system, we demonstrated that dkk1, shown as a heart inducer in this system, has a strong ability to induce the expression of POX2. Injection of a high dose dkk1 RNA induced a heart marker while a low dose of dkk1 preferentially induced the expression of POX2, suggesting that dkk1 works as a morphogen to determine the different lineages. Overall results indicate that wnt signal inhibitors induce leukocytes at the early neurula stage and that these cells spread to the entire body and exist until the ventral blood island-derived leukocytes appear in the body.

Animals↗
PubMed1991

Properties of ionic currents induced by external ATP in a mouse mesodermal stem cell line.

1. ATP was puff applied to cells of a mesodermal stem cell line, C3H10T1/2, and the responses were studied by whole-cell patch clamp recording. 2. In 91% of the cells (90/99), K+ current lasting for tens of seconds was observed after several seconds latency. The current showed outward rectification. In 10% of the cells (9/99), ATP induced Cl- current which also lasted for tens of seconds after several seconds latency, but showed little rectification. In 6% of these cells (5/99), both K+ and Cl- currents were induced by ATP. 3. The K+ current induced by ATP was dose dependent, with a Kd of 0.4 microM. The effects of ATP analogues were tested at a concentration of 20 microM. ADP and ATP-gamma-S induced the K+ current, while AMP and adenosine did not. alpha, beta-Methylene ATP produced a diminished K+ current. 4. The ATP-induced K+ current was not observed when EGTA in the internal solution was raised from 0.1 to 5 mM. In Fluo-3-loaded cells, an increase in intracellular Ca2+ concentration induced by the application of ATP was observed, and the time course was similar to the induced K+ current. Both the increase in intracellular Ca2+ and the K+ current were induced by ATP even in Ca(2+)-free external solution. Ryanodine (50 microM) in the external solution did not affect the ATP response, and application of 10 mM-caffeine alone to the external solution did not induce any response. 5. The variance of the steady-state fluctuations in the course of the ATP-induced slow K+ current was analysed. The single-channel conductance was estimated as 2.7 pS at 0 mV with external and internal K+ concentrations of 5 and 140 mM respectively. The K+ current was not affected by apamin at concentrations of up to 1 microM but was reduced to one-third by 140 mM-tetraethylammonium (TEA). 6. It was concluded that puff-applied ATP has two main effects in the mesodermal stem cells: an increase in the intracellular Ca2+ concentration and a succeeding hyperpolarization due to the Ca(2+)-activated K+ conductance which is present in this cell. The significance of the increase in intracellular Ca2+ caused by ATP is discussed.

Adenosine Triphosphate↗
PubMed2001

Switching repulsion to attraction: changing responses to slit during transition in mesoderm migration.

Slit is secreted by cells at the midline of the central nervous system, where it binds to Roundabout (Robo) receptors and functions as a potent repellent. We found that migrating mesodermal cells in vivo respond to Slit as both an attractant and a repellent and that Robo receptors are required for both functions. Mesoderm cells expressing Robo receptors initially migrate away from Slit at the midline. A few hours after migration, these same cells change their behavior and require Robo to extend toward Slit-expressing muscle attachment sites. Thus, Slit functions as a chemoattractant to provide specificity for muscle patterning.

Animals↗
PubMed2001

Patterns of gene expression during Drosophila mesoderm development.

The transcription factor Twist initiates Drosophila mesoderm development, resulting in the formation of heart, somatic muscle, and other cell types. Using a Drosophila embryo sorter, we isolated enough homozygous twist mutant embryos to perform DNA microarray experiments. Transcription profiles of twist loss-of-function embryos, embryos with ubiquitous twist expression, and wild-type embryos were compared at different developmental stages. The results implicate hundreds of genes, many with vertebrate homologs, in stage-specific processes in mesoderm development. One such gene, gleeful, related to the vertebrate Gli genes, is essential for somatic muscle development and sufficient to cause neural cells to express a muscle marker.

Animals↗
PubMed1994

Induction of mesoderm in Xenopus laevis embryos by translation initiation factor 4E.

The microinjection of messenger RNA encoding the eukaryotic translation initiation factor 4E (eIF-4E) into early embryos of Xenopus laevis leads to the induction of mesoderm in ectodermal explants. This induction occurs without a stimulation of overall protein synthesis and is blocked by the co-expression of a dominant negative mutant of the proto-oncogene ras or a truncated activin type II receptor. Although other translation factors have been studied in vertebrate and invertebrate embryos, none have been shown to play a direct role in development. The results here suggest a mechanism for relaying and amplifying signals for mesoderm induction.

Animals↗
PubMed1998

Structural determinants of SHP-2 function and specificity in Xenopus mesoderm induction.

SHP-2 is a positive component of many receptor tyrosine kinase signaling pathways. The related protein-tyrosine phosphatase (PTP) SHP-1 usually acts as a negative regulator. The precise domains utilized by SHP-2 to transmit positive signals in vivo and the basis for specificity between SHP-1 and SHP-2 are not clear. In Xenopus, SHP-2 is required for mesoderm induction and completion of gastrulation. We investigated the effects of SHP-2 mutants and SHP-2/SHP-1 chimeras on basic fibroblast growth factor-induced mesoderm induction. Both SH2 domains and the PTP domain are required for normal SHP-2 function in this pathway. The N-terminal SH2 domain is absolutely required, whereas the C-terminal SH2 contributes to wild-type function. The C-terminal tyrosyl phosphorylation sites and proline-rich region are dispensable, arguing against adapter models of SHP-2 function. Although the SH2 domains contribute to SHP-2 specificity, studies of SHP chimeras reveal that substantial specificity resides in the PTP domain. Thus, PTP domains exhibit biologically relevant specificity in vivo, and noncatalytic and catalytic domains of PTPs contribute to specificity in a combinatorial fashion.

Animals↗
PubMed2003

The murine Nck SH2/SH3 adaptors are important for the development of mesoderm-derived embryonic structures and for regulating the cellular actin network.

Mammalian Nck1 and Nck2 are closely related adaptor proteins that possess three SH3 domains, followed by an SH2 domain, and are implicated in coupling phosphotyrosine signals to polypeptides that regulate the actin cytoskeleton. However, the in vivo functions of Nck1 and Nck2 have not been defined. We have mutated the murine Nck1 and Nck2 genes and incorporated beta-galactosidase reporters into the mutant loci. In mouse embryos, the two Nck genes have broad and overlapping expression patterns. They are functionally redundant in the sense that mice deficient for either Nck1 or Nck2 are viable, whereas inactivation of both Nck1 and Nck2 results in profound defects in mesoderm-derived notochord and embryonic lethality at embryonic day 9.5. Fibroblast cell lines derived from Nck1(-/-) Nck2(-/-) embryos have defects in cell motility and in the organization of the lamellipodial actin network. These data suggest that the Nck SH2/SH3 adaptors have important functions in the development of mesodermal structures during embryogenesis, potentially linked to a role in cell movement and cytoskeletal organization.

Actins↗
PubMed1975

Sclero-cornea and defective mesodermal migration.

A 5-month-old boy with bilateral sclero-cornea, multiple systemic abnormalities, and normal karyotype had his left eye removed after corneal perforation. Histopathological examination of the enucleated eye revealed an irregular corneal epithelium, absent Bowman's membrane, thickened and vascularized stromal lamellae, absent Descemet's membrane and endothelium, no angle structures, hypoplasia of the iris and ciliary body, and total kerato-iridic adhesions. A profound defect in embryogenesis due to defective mesodermal migration during the earliest phase of mesoderm differentiation is postulated as the causative factor in this case.

Choroid↗
PubMed1999

Malignant mixed mesodermal tumors of the ovary: preoperative diagnosis.

Early diagnosis of malignant mixed mesodermal tumors of the ovary is very difficult because of the rarity and the insidious onset. The purpose of this report is to review the magnetic resonance imaging features of an ovarian malignant mixed mesodermal tumor, which occurred in a 52-year-old woman, aiding in the differential diagnosis.

Chemotherapy, Adjuvant↗
PubMed1987

Ultrastructural analysis of chick embryo blastoderms explanted in vitro in absence of endoderm. Differentiation capacity of mesoderm.

A study of the structural characteristics of stage 5 chick embryo blastoderms, cultured in vitro, was carried out after previous elimination of endoderm to analyse the differentiation capacity of mesoderm. Our results show that only the precardiac mesoderm is determined at this early stage and that it is able to differentiate cardiac tissue in the absence of the endoderm. The ultrastructural characteristics of this tissue are described. However, the degree of differentiation of cardiomyoblasts does not reach the expected level of organization and myofibrillar complexity.

Animals↗
PubMedDate not supplied

Mesodermal induction defect as a possible cause of ear malformations.

Deafness due to inner ear anomalies is rarely associated with malformations of the auricles. We describe two brothers with profound congenital sensorineural deafness, abnormal vestibular function, normal ossicles, and delayed motor development. Since the external and inner ear originate from distinctly separate structures, the embryogenesis of this malformation association is less clear than in the more common association of external and middle anomalies, where the latter two structures are derived from the first and second branchial arches. The combination of auricular and inner ear anomalies, with sparing of the middle ear structures, can be explained on the assumption that mesodermal induction is responsible for normal differentiation of both the otocyst and of the branchial arch ectoderm. A recessive mutant gene may lead to a deficiency of a mesodermal inducer substance of a target tissue receptor site. A similar mechanism may be involved in other multiple malformation syndromes, whereby a mutant gene acting during a specific period of organogenesis causes disruption of the normal induction-competence relationship.

Cell Differentiation↗