The Experts below are selected from a list of 10188 Experts worldwide ranked by ideXlab platform
Charles A Ettensohn - One of the best experts on this subject based on the ideXlab platform.
-
Growth factor-mediated Mesodermal Cell guidance and skeletogenesis during sea urchin gastrulation.
2018Co-Authors: Ashrifia Adomako-ankomah, Charles A EttensohnAbstract:Growth factor signaling pathways provide essential cues to mesoderm Cells during gastrulation in many metazoans. Recent studies have implicated the VEGF and FGF pathways in providing guidance and differentiation cues to primary mesenchyme Cells (PMCs) during sea urchin gastrulation, although the relative contributions of these pathways and the Cell behaviors they regulate are not fully understood. Here, we show that FGF and VEGF ligands are expressed in distinct domains in the embryonic ectoderm of Lytechinus variegatus. We find that PMC guidance is specifically disrupted in Lv-vegf3 morphants and these embryos fail to form skeletal elements. By contrast, PMC migration is unaffected in Lv-fgfa morphants, and well-patterned but shortened skeletal elements form. We use a VEGFR inhibitor, axitinib, to show that VEGF signaling is essential not only for the initial phase of PMC migration (subequatorial ring formation), but also for the second phase (migration towards the animal pole). VEGF signaling is not required, however, for PMC fusion. Inhibition of VEGF signaling after the completion of PMC migration causes significant defects in skeletogenesis, selectively blocking the elongation of skeletal rods that support the larval arms, but not rods that form in the dorsal region of the embryo. Nanostring nCounter analysis of ∼100 genes in the PMC gene regulatory network shows a decrease in the expression of many genes with proven or predicted roles in biomineralization in vegf3 morphants. Our studies lead to a better understanding of the roles played by growth factors in sea urchin gastrulation and skeletogenesis.
-
lvdelta is a mesoderm inducing signal in the sea urchin embryo and can endow blastomeres with organizer like properties
Development, 2002Co-Authors: Hyla C Sweet, Michael Gehring, Charles A EttensohnAbstract:Signals from micromere descendants play a critical role in patterning the early sea urchin embryo. Previous work demonstrated a link between the induction of mesoderm by micromere descendants and the Notch signaling pathway. In this study, we demonstrate that these micromere descendants express LvDelta, a ligand for the Notch receptor. LvDelta is expressed by micromere descendants during the blastula stage, a time when signaling has been shown to occur. By a combination of embryo microsurgery, mRNA injection and antisense morpholino experiments, we show that expression of LvDelta by micromere descendants is both necessary and sufficient for the development of two Mesodermal Cell types, pigment Cells and blastocoelar Cells. We also demonstrate that LvDelta is expressed by macromere descendants during mesenchyme blastula and early gastrula stages. Macromere-derived LvDelta is necessary for blastocoelar Cell and muscle Cell development. Finally, we find that expression of LvDelta is sufficient to endow blastomeres with the ability to function as a vegetal organizing center and to coordinate the development of a complete pluteus larva.
-
Mesodermal Cell interactions in the sea urchin embryo properties of skeletogenic secondary mesenchyme Cells
Development, 1993Co-Authors: Charles A Ettensohn, Seth RuffinsAbstract:An interaction between the two principal populations of Mesodermal Cells in the sea urchin embryo, primary and secondary mesenchyme Cells (PMCs and SMCs, respectively), regulates SMC fates and the process of skeletogenesis. In the undisturbed embryo, skeletal elements are produced exclusively by PMCs. Certain SMCs also have the ability to express a skeletogenic phenotype; however, signals transmitted by the PMCs direct these Cells into alternative developmental pathways. In this study, a combination of fluorescent Cell-labeling methods, embryo microsurgery and Cell-specific molecular markers have been used to study the lineage, numbers, normal fate(s) and developmental potential of the skeletogenic SMCs. Previous fate-mapping studies have shown that SMCs are derived from the veg2 layer of blastomeres of the 64-Cell-stage embryo and from the small micromeres. By specifically labeling the small micromeres with 5-bromodeoxyuridine, we demonstrate that descendants of these Cells do not participate in skeletogenesis in PMC-depleted larvae, even though they are the closest lineal relatives of PMCs. Skeletogenic SMCs are therefore derived exclusively from the veg2 blastomeres. Because the SMCs are a heterogeneous population of Cells, we have sought to gain information concerning the normal fate(s) of skeletogenic SMCs by determining whether specific Cell types are reduced or absent in PMC(−) larvae. Of the four known SMC derivatives: pigment Cells, blastocoelar (basal) Cells, muscle Cells and coelomic pouch Cells, only pigment Cells show a major reduction (> 50%) in number following SMC skeletogenesis. We therefore propose that the PMC-derived signal regulates a developmental switch, directing SMCs to adopt a pigment Cell phenotype instead of a default (skeletogenic) fate. Ablation of SMCs at the late gastrula stage does not result in the recruitment of any additional skeletogenic Cells, demonstrating that, by this stage, the number of SMCs with skeletogenic potential is restricted to 60–70 Cells. Previous studies showed that during their switch to a skeletogenic fate, SMCs alter their migratory behavior and Cell surface properties. In this study, we demonstrate that during conversion, SMCs become insensitive to the PMC-derived signal, while at the same time they acquire PMC-specific signaling properties.
-
Cell interactions and Mesodermal Cell fates in the sea urchin embryo
Development, 1992Co-Authors: Charles A EttensohnAbstract:Cell interactions during gastrulation play a key role in the determination of Mesodermal Cell fates in the sea urchin embryo. An interaction between primary and secondary mesenchyme Cells (PMCs and SMCs, respectively), the two principal populations of Mesodermal Cells, regulates the expression of SMC fates. PMCs are committed early in cleavage to express a skeletogenic phenotype. During gastrulation, they transmit a signal that suppresses the skeletogenic potential of a subpopulation of SMCs and directs these Cells into an alternative developmental pathway. This review summarizes present information concerning the Cellular basis of the PMC-SMC interaction, as analyzed by Cell transplantation and ablation experiments, fluorescent Cell labeling methods and the use of Cell type-specific molecular markers. The nature and stability of SMC fate switching, the timing of the PMC-SMC interaction and its quantitative characteristics, and the lineage, numbers and normal fate of the population of skeletogenic SMCs are discussed. Evidence is presented indicating that PMCs and SMCs come into direct filopodial contact during the late gastrula stage, when the signal is transmitted. Finally, evolutionary questions raised by these studies are briefly addressed.
Ursula Just - One of the best experts on this subject based on the ideXlab platform.
-
activated notch1 alters differentiation of embryonic stem Cells into Mesodermal Cell lineages at multiple stages of development
Mechanisms of Development, 2006Co-Authors: Timm Schroeder, Franziska Meierstiegen, Ralf Schwanbeck, Hanna M Eilken, Satomi Nishikawa, Robert Hasler, Stefan Schreiber, Georg W Bornkamm, Shinichi Nishikawa, Ursula JustAbstract:Abstract Signals of Notch transmembrane receptors function to regulate a wide variety of developmental Cell fates. Here we investigate the role of Notch signaling in the development of Mesodermal Cell types by expressing a tamoxifen-inducible, activated form of Notch1 in embryonic stem Cells (ESC). For differentiation of ESC into first Mesodermal progenitor Cells and then endothelial, mural, cardiac muscle and hematopoietic Cells, the OP9 stroma co-culture system was used. Timed activation of Notch signaling by the addition of tamoxifen at various stages during differentiation of ESC into Mesodermal Cell lineages results in profound alterations in the generation of all of these Cells. Differentiation of ESC into Flk1+ Mesodermal Cells is inhibited by activated Notch. When Notch signaling is activated in Mesodermal Cells, generation of cardiac muscle, endothelial and hematopoietic Cells is inhibited, favoring the generation of mural Cells. Activation of Notch signaling in hematopoietic Cells reduces colony formation and maintenance of hematopoiesis. These data suggest that Notch signaling plays a regulatory role in Mesodermal development, cardiomyogenesis, the balanced generation of endothelial versus mural Cells of blood vessels and hematopoietic development.
-
Recombination signal sequence-binding protein Jκ alters Mesodermal Cell fate decisions by suppressing cardiomyogenesis
Proceedings of the National Academy of Sciences of the United States of America, 2003Co-Authors: Timm Schroeder, Satomi Nishikawa, Georg W Bornkamm, Shinichi Nishikawa, Stuart T. Fraser, Minetaro Ogawa, Chio Oka, Tasuku Honjo, Ursula JustAbstract:The transcription factor recombination signal sequence-binding protein Jκ (RBP-J) is a key downstream element in the signaling pathway of all four mammalian Notch receptors that are critically involved in the control of embryonic and adult development. RBP-J-deficient mice display complex defects and die around day 9.5 postcoitum. Here, we investigate the function of RBP-J in the development of Mesodermal Cell lineages by using the OP9 stroma coculture system. RBP-J-deficient embryonic stem (ES) Cells gave rise to cardiomyocytes, endothelial Cells, and primitive and definitive hematopoietic Cells. Thus, RBP-J-mediated signals are not required for generation of these Cell types. However, when compared with parental RBP-J-expressing ES Cells, cardiomyogenesis derived from RBP-J-deficient ES Cells was increased. Repression over the cardiogenic pathway was restored by expressing RBP-J in RBP-J-deficient ES Cells. Our data indicate that Notch signaling via RBP-J plays an important role for the correct specification of myocardial Cell fates.
Masaki Noda - One of the best experts on this subject based on the ideXlab platform.
-
Noggin Inhibits Chondrogenic But Not Osteogenic Differentiation in Mesodermal Stem Cell Line C1 and Skeletal Cells
Endocrinology, 2004Co-Authors: Akira Nifuji, Odile Kellermann, Masaki NodaAbstract:Osteoblasts and chondroblasts are derived from common mesenchymal progenitors. Although bone morphogenetic protein induces mesenchymal differentiation into both osteogenic and chodrogenic lineage Cells in vitro, its inhibitor, Noggin, is expressed exclusively during chondrogenic but not osteogenic differentiation in an embryonal carcinoma-derived Mesodermal Cell line, C1. We hypothesized that Noggin may regulate Cell differentiation in a lineage-specific manner. To test this hypothesis, Noggin was overexpressed using recombinant adenovirus (Ad/Noggin) in Mesodermal C1 Cells to examine whether Noggin specifically inhibits chondrogenic differentiation. Noggin overexpression by recombinant adenovirus infection reduced Sox9, patched, Ihh, and type II, X, and XI collagen mRNA expression levels in C1 Cell aggregates that were induced to differentiate into chondrocyte lineage by culturing in differentiation medium. In contrast, Noggin overexpression did not affect osteogenic differentiation in C1 Cells because osteoblast phenotypic markers such as osteocalcin and alkaline phosphatase mRNA levels were not altered. We further examined whether Noggin also differentially affects chondrogenesis and osteogenesis in limb development by using organ cultures of long bone. Ad/Noggin infection into 15.5 d post conception limb skeletal rudiments that were cultured on filter membrane in vitro or on the chorioallantoic membranes in ovo inhibited the levels of chondrogenesis, which were evaluated based on alcian blue staining. These results suggest that Noggin specifically blocks chondrogenic differentiation, rather than osteogenic differentiation, in Mesodermal stem Cell line C1 and skeletal Cells.
-
bone morphogenetic protein regulation of forkhead winged helix transcription factor foxc2 mfh1 in a murine Mesodermal Cell line c1 and in skeletal precursor Cells
Journal of Bone and Mineral Research, 2001Co-Authors: Akira Nifuji, Odile Kellermann, Naoyuki Miura, Naoko Kato, Masaki NodaAbstract:Mfh1/Foxc2 is a member of forkhead/winged helix transcription factor family in which its members serve as key regulators in embryogenesis and Cell differentiation in various species. Mutant mice null for Mfh1 show defects in axial and cranial skeletogenesis, suggesting requirement of Mfh1 for skeletal tissue development. However, the roles of Mfh1 and its regulation during early skeletogenesis have not been understood fully yet. In this study, we investigated developmental regulation of Mfh1 expression during embryonic skeletogenesis in vivo and in vitro chondrogenic Cell differentiation using a Mesodermal progenitor-like Cell line C1. We first examined expression patterns of Mfh1 in relation to the cartilage phenotype-related molecules including bone morphogenetic proteins (BMPs) during mouse embryogenesis by in situ hybridization. In 10.5 days postcoitum (dpc) mouse limb, Mfh1 messenger RNA (mRNA) was expressed in the mesenchymal Cells in the tissues that later give rise to skeleton. In 11.5 dpc embryos, Mfh1 transcripts were expressed in the Cell condensation of skeletal blastemas. BMP2 transcripts were expressed in the Cell condensation proximal to the Mfh1-expressing Cells in the limbs and those of BMP-7 were expressed in the mesenchymal tissue surrounding the Mfh1-positive Cell condensation. In 12.5 dpc and 13.5 dpc embryos, the expression of Mfh1 was localized to the perichondrium, which surrounds Cells that express noggin and SOX9 mRNA. BMP-2 expression was overlapped with that of Mfh1 in the peripheral layer of 12.5 dpc and 13.5 dpc limb skeletal blastemas. Mfh1 expression persisted in the perichondrium of 15.5 dpc embryos though its level was reduced. We then examined the expression of Mfh1 in the mouse Mesodermal Cell line C1 that differentiates into chondrocytes in vitro. Mfh1 mRNA was expressed constitutively at low levels in C1 Cells before the induction of its differentiation. On the differentiation of C1 Cells into chondrocytes by the treatment with dexamethasone (Dex), Mfh1 expression was increased and peaked on day 4 of Dex treatment. Treatment with BMP-4/7 and BMP-7 protein also enhanced Mfh1 expression in C1 Cells. To further examine the causative relationship between BMP and Mfh1 in mesenchymal tissue, we performed a mouse limb bud organ culture to implant BMP proteins with carriers into the mesenchymal tissue of the limb bud. Implantation of BMP-7 protein in the limb bud of 11.5 dpc embryos induced Mfh1 expression, suggesting that BMP regulates Mfh1 expression in limb mesenchyme. These results indicate that Mfh1 expression is associated with the early stage of chondrogenic differentiation both in vivo and in vitro and that BMPs regulate Mfh1 expression in skeletal precursor Cells.
-
noggin expression in a Mesodermal pluripotent Cell line c1 and its regulation by bmp
Journal of Cellular Biochemistry, 1999Co-Authors: Akira Nifuji, Odile Kellermann, Masaki NodaAbstract:Osteoblasts and chondrocytes are derived from Mesodermal stem Cells and their differentiation is under the control of coordinated interaction among signaling molecules. Noggin is one of the signaling molecules which bind to and inactivate BMPs to induce neural tissues and dorsal mesoderm in Xenopus. However, its expression and regulation in mammalian Cells has not been known. In this study, we investigated expression of noggin in murine pluripotent Mesodermal Cell line, C1. Noggin expression was very low in these C1 Cells before they were induced to differentiate. When C1 Cells were induced to differentiate into chondrocytes in aggregate cultures in the presence of dexamethasone(dex), noggin expression was significantly increased. In a sharp contrast, when the C1 Cells were induced to differentiate into osteoblastic Cells by the treatment with beta glycerophosphate (betaGP) and ascorbic acid (AA), noggin mRNA expression remained to be barely detectable. Noggin expression was also observed in the developing cartilage of vertebrae in 15.5 dpc mouse embryos. The noggin mRNA level in C1 Cells in monolayer cultures was enhanced significantly by the treatment with BMP4/7 in a dose-dependent manner with a maximal effect at 100 ng/ml. The BMP4/7 effect on noggin expression was time dependent starting within 12 h and peaked at 24 h. These results indicate that noggin is expressed in the pluripotent Mesodermal Cell line C1 and that its expression is regulated by BMP.
Thierry Darribere - One of the best experts on this subject based on the ideXlab platform.
-
a key function for αv containing integrins in Mesodermal Cell migration duringpleurodeles waltlgastrulation
Developmental Biology, 1998Co-Authors: Mylene Skalski, Dominique Alfandari, Thierry DarribereAbstract:Abstract During cleavage ofPleurodeles waltlamphibian embryos, inner Cells of the blastocoel roof (presumptive ectodermal and Mesodermal Cells) organize a fibrillar extraCellular matrix (ECM) containing fibronectin on their basal surface by a β1-integrin-dependent process. This matrix is used as a migratory substrate by Mesodermal Cells during gastrulation. While α5β1 integrin is expressed on both ectodermal and Mesodermal Cell surface, we have shown previously that αv containing integrins are essentially restricted to the surface of Mesodermal Cells (Alfandari, D., Whittaker, C. A., DeSimone, D. W., and Darribere, T.,Dev. Biol.170, 249–261, 1995). To investigate the function of αv integrins during gastrulation, we have generated a function blocking antibody directed against the extraCellular domain of thePleurodelesintegrin αv subunit. The antibody did not prevent fibronectin fibril formation, whereas an antibody against the α5β1 integrin did. When injected into the blastocoel, the antibody against integrin αv subunit perturbed gastrulation and further development in a stage-dependent manner. Developmental defects were correlated to an abnormal positioning of the mesoderm layer.In vitro,the antibody blocked spreading of Mesodermal Cell to fibronectin or blastocoel roof ECM but not their attachment. In contrast, the antibody directed against the α5β1 integrin inhibited both Cell attachment and spreading to the same substrates. We propose that the α5β1 integrin is required for fibronectin assembly into fibrils and Mesodermal Cell attachment to the blastocoel roof ECM, while the αv containing integrins are necessary for Cell spreading, and possibly migration, on this complex network.
-
integrin alpha v subunit is expressed on Mesodermal Cell surfaces during amphibian gastrulation
Developmental Biology, 1995Co-Authors: Dominique Alfandari, Charles A Whittaker, Douglas W Desimone, Thierry DarribereAbstract:Abstract Mesodermal Cell migration during amphibian gastrulation is dependent on Cellular interactions with fibronectin. One mechanism whereby Cells bind fibronectin is through αv-containing integrin heterodimers. In order to investigate the role of αv in amphibian gastrulation, we have cloned the Pleurodeles homologue of the integrin αv subunit using homology PCR. The deduced amino acid sequence is 73 and 74% identical with the human and chick homologues, respectively. The 4.8-kb mRNA is expressed during oogenesis and persists throughout development. Messenger RNA and protein are widely expressed in oocytes and embryos while Cell surface expression is spatially regulated. The protein first appears on the plasma membrane of fully grown oocytes. Fertilization results in the progressive loss of αv membrane localization. Before and during gastrulation, the integrin αv subunit is expressed on the surface of Mesodermal Cells. These data show that αv expression is developmentally regulated by a post-translational mechanism which correlates with the onset of Mesodermal Cell migration at gastrulation.
-
Mesodermal Cell adhesion to fibronectin rich fibrillar extraCellular matrix is required for normal rana pipiens gastrulation
Journal of Experimental Zoology, 1993Co-Authors: Kurt E Johnson, Thierry Darribere, Jeanclaude BoucautAbstract:New observations on thin strips of Cells from the leading edge of the involuting presumptive mesoderm explanted onto FN-coated substrata show a striking preferential Cellular emigration from the leading edge of explants. Microinjected probes (Fab′ anti-FN, Fab' anti-integrin and RGD-peptides) that disrupt Cell adhesion to the FN-matrix on basal surface of the blastocoel roof also disrupt normal anuran gastrulation, producing blocked embryos with no adhesion of leading edge Mesodermal Cells to the blastocoel roof, abnormal epiboly, and defects of Mesodermal Cell spreading across the basal surface of the blastocoel roof toward the animal pole. These results show that the FN-rich fibrillar extraCellular matrix on the basal surface of the blastocoel roof is required for normal gastrulation in Rana pipiens embryos. © 1993 Wiley-Liss, Inc.
-
amphibian gastrulation the molecular bases of Mesodermal Cell migration in urodele embryos
1991Co-Authors: Jeanclaude Boucaut, Jeanfrancois Riou, Thierry Darribere, Kurt E Johnson, D L Shi, Michel DelarueAbstract:During the early developmental period of the vertebrate embryo, called gastrulation, changes in Cell shape, Cell number, and Cell-Cell associations produce fundamental changes in embryonic morphology. Selected populations of Cells are designated to perform particular ensembles of Cell movements. Typically, morphogenetic Cell movements are regulated in a repeatable pattern from embryo to embryo. These morphogenetic Cell movements lead to the organization of an embryo with three primary germ layers: ectoderm, mesoderm, and endoderm. It is difficult enough to understand how Cells move from one location to another inside the embryo but even more mysterious why they choose one particular pathway for this locomotion from among the large number of pathways theoretically available to them.
Pedro Martinez - One of the best experts on this subject based on the ideXlab platform.
-
Mesodermal Gene Expression in the Acoel Isodiametra pulchra Indicates a Low Number of Mesodermal Cell Types and the EndoMesodermal Origin of the Gonads
PLOS ONE, 2013Co-Authors: Marta Chiodin, Peter Ladurner, Aina Børve, Eugene Berezikov, Pedro MartinezAbstract:Acoelomorphs are bilaterally symmetric small marine worms that lack a coelom and possess a digestive system with a single opening. Two alternative phylogenetic positions of this group within the animal tree are currently debated. In one view, Acoelomorpha is the sister group to all remaining Bilateria and as such, is a morphologically simple stepping stone in bilaterian evolution. In the other, the group is a lineage within the Deuterostomia, and therefore, has derived a simple morphology from a more complex ancestor. Acoels and the closely related Nemertodermatida and Xenoturbellida, which together form the Acoelomorpha, possess a very limited number of Cell types. To further investigate the diversity and origin of Mesodermal Cell types we describe the expression pattern of 12 orthologs of bilaterian Mesodermal markers including Six1/2, Twist, FoxC, GATA4/5/6, in the acoel Isodiametra pulchra. All the genes are expressed in stem Cells (neoblasts), gonads, and at least subsets of the acoel musculature. Most are expressed in endoMesodermal compartments of I. pulchra developing embryos similar to what has been described in cnidarians. Our molecular evidence indicates a very limited number of Mesodermal Cell types and suggests an endoMesodermal origin of the gonads and the stem Cell system. We discuss our results in light of the two prevailing phylogenetic positions of Acoelomorpha.