Xwnt-8, a Xenopus Wnt-1/int-1-related gene responsive to mesoderm-inducing growth factors, may play a role in ventral mesodermal patterning during embryogenesis

Development ◽  
1991 ◽  
Vol 111 (4) ◽  
pp. 1045-1055 ◽  
Author(s):  
J.L. Christian ◽  
J.A. McMahon ◽  
A.P. McMahon ◽  
R.T. Moon
Keyword(s):  
Growth Factors ◽  
Cell Fate ◽  
Ectopic Expression ◽  
Mesoderm Induction ◽  
Related Gene ◽  
Mesodermal Cell ◽  
Peptide Growth Factors ◽  
Basic Body ◽  
Inducing Factors ◽  
Mesoderm Inducing Factors

In amphibian embryos, formation of the basic body plan depends on positional differences in the mesoderm. Although peptide growth factors involved in mesoderm induction have tentatively been identified, additional signals are required to generate pattern in this tissue. We have isolated a Xenopus cDNA for a Wnt-1 related gene, designated Xwnt-8, which is activated in response to mesoderm-inducing growth factors. Xwnt-8 transcripts are transiently expressed, being most abundant during gastrulation at which time expression is confined primarily to ventral mesodermal cells. Embryos dorsoanteriorized by exposure to lithium exhibit greatly reduced levels of Xwnt-8 mRNA, supporting a correlation between Xwnt-8 expression and a ventral mesodermal cell fate. Surprisingly, ectopic expression of Xwnt-8 in embryos causes a dorsoanterior-enhanced phenotype. These findings suggest that Xwnt-8 may be a secondary signalling agent which is produced in response to mesoderm-inducing factors and is involved in the early steps of mesodermal patterning.

DVR-4 (bone morphogenetic protein-4) as a posterior-ventralizing factor in Xenopus mesoderm induction

Development ◽  
1992 ◽  
Vol 115 (2) ◽  
pp. 639-647 ◽  
Author(s):  
C.M. Jones ◽  
K.M. Lyons ◽  
P.M. Lapan ◽  
C.V. Wright ◽  
B.L. Hogan
Keyword(s):  
Growth Factors ◽  
Bone Morphogenetic Protein ◽  
Ectopic Expression ◽  
Body Plan ◽  
Bone Morphogenetic Protein 4 ◽  
Mesoderm Induction ◽  
Tgf Beta ◽  
Signalling Molecules ◽  
Morphogenetic Protein ◽  
Peptide Growth Factors

Establishment of mesodermal tissues in the amphibian body involves a series of inductive interactions probably elicited by a variety of peptide growth factors. Results reported here suggest that mesodermal patterning involves an array of signalling molecules including DVR-4, a TGF-beta-like molecule. We show that ectopic expression of DVR-4 causes embryos to develop with an overall posterior and/or ventral character, and that DVR-4 induces ventral types of mesoderm in animal cap explants. Moreover, DVR-4 overrides the dorsalizing effects of activin. DVR-4 is therefore the first molecule reported both to induce posteroventral mesoderm and to counteract dorsalizing signals such as activin. Possible interactions between these molecules resulting in establishment of the embryonic body plan are discussed.

FGF is a prospective competence factor for early activin-type signals in Xenopus mesoderm induction

Development ◽  
1995 ◽  
Vol 121 (8) ◽  
pp. 2429-2437 ◽  
Author(s):  
R.A. Cornell ◽  
T.J. Musci ◽  
D. Kimelman
Keyword(s):  
Ectopic Expression ◽  
Equatorial Region ◽  
Mesoderm Induction ◽  
Normal Pattern ◽  
Fgf Receptor ◽  
Competence Factor ◽  
Low Levels ◽  
Inducing Factors ◽  
Mesoderm Inducing Factors ◽  
Cellular Competence

Normal pattern formation during embryonic development requires the regulation of cellular competence to respond to inductive signals. In the Xenopus blastula, vegetal cells release mesoderm-inducing factors but themselves become endoderm, suggesting that vegetal cells may be prevented from expressing mesodermal genes in response to the signals that they secrete. We show here that addition of low levels of basic fibroblast growth factor (bFGF) induces the ectopic expression of the mesodermal markers Xbra, MyoD and muscle actin in vegetal explants, even though vegetal cells express low levels of the FGF receptor. Activin, a potent mesoderm-inducing agent in explanted ectoderm (animal explants), does not induce ectopic expression of these markers in vegetal explants. However, activin-type signaling is present in vegetal cells, since the vegetal expression of Mix.1 and goosecoid is inhibited by the truncated activin receptor. These results, together with the observation that FGF is required for mesoderm induction by activin, support our proposal that a maternal FGF acts at the equator as a competence factor, permitting equatorial cells to express mesoderm in response to an activin-type signal. The overlap of FGF and activin-type signaling is proposed to restrict mesoderm to the equatorial region.

scholarly journals Tet proteins influence the balance between neuroectodermal and mesodermal fate choice by inhibiting Wnt signaling

2016 ◽  
Vol 113 (51) ◽  
pp. E8267-E8276 ◽  
Author(s):  
Xiang Li ◽  
Xiaojing Yue ◽  
William A. Pastor ◽  
Lizhu Lin ◽  
Romain Georges ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Cell Fate ◽  
Transcriptional Activation ◽  
Ectopic Expression ◽  
Embryonic Stem ◽  
Mesodermal Cell ◽  
Cell Fate Decisions ◽  
Tet Proteins ◽  
Mesoderm Specification ◽  
Wnt Inhibitor

TET-family dioxygenases catalyze conversion of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) and oxidized methylcytosines in DNA. Here, we show that mouse embryonic stem cells (mESCs), either lacking Tet3 alone or with triple deficiency of Tet1/2/3, displayed impaired adoption of neural cell fate and concomitantly skewed toward cardiac mesodermal fate. Conversely, ectopic expression of Tet3 enhanced neural differentiation and limited cardiac mesoderm specification. Genome-wide analyses showed that Tet3 mediates cell-fate decisions by inhibiting Wnt signaling, partly through promoter demethylation and transcriptional activation of the Wnt inhibitor secreted frizzled-related protein 4 (Sfrp4). Tet1/2/3-deficient embryos (embryonic day 8.0–8.5) showed hyperactivated Wnt signaling, as well as aberrant differentiation of bipotent neuromesodermal progenitors (NMPs) into mesoderm at the expense of neuroectoderm. Our data demonstrate a key role for TET proteins in modulating Wnt signaling and establishing the proper balance between neural and mesodermal cell fate determination in mouse embryos and ESCs.

scholarly journals The Xenopus MyoD gene: an unlocalised maternal mRNA predates lineage-restricted expression in the early embryo

Development ◽  
1990 ◽  
Vol 108 (4) ◽  
pp. 669-680 ◽  
Author(s):  
R.P. Harvey
Keyword(s):  
Gene Expression ◽  
Cultured Cells ◽  
Early Response ◽  
Early Embryo ◽  
Mesoderm Induction ◽  
Animal Pole ◽  
Early Expression ◽  
Inducing Factors ◽  
Mesoderm Inducing Factors ◽  
Myod Gene

Expression of the mouse MyoD gene appears to represent a critical point in the commitment of cultured cells to muscle. In Xenopus, myogenic commitment begins during mesoderm induction which is initiated early in development by endogenous growth factors. To study MyoD gene expression during induction, a Xenopus MyoD gene and homologous cDNAs were selected from Xenopus libraries and analysed. Two different cDNAs have been sequenced. They code for proteins closely related to each other and to mouse MyoD and are likely to be expressed from duplicated Xenopus MyoD genes. Surprisingly, MyoD mRNA is first detected during oogenesis and the maternal species is not localized exclusively to the region of the blastula fated to muscle. Zygotic MyoD mRNA accumulates slowly above maternal levels beginning at the MBT and new transcripts are localized to the somitic mesoderm. Expression outside of somites has been detected in developing heads of tailbud embryos and can be induced in blastula animal pole explants treated with mesoderm-inducing factors. The early expression of MyoD in Xenopus development suggests that it may play a part in the induction of muscle mesoderm and generally strengthens the evidence that MyoD is determinative in muscle commitment. In addition, the initiation of MyoD transcription at the MBT and its stimulation by mesoderm-inducing factors implies that MyoD gene expression is an immediate early response to mesoderm induction.

scholarly journals Sox2 and canonical Wnt signaling interact to activate a developmental checkpoint coordinating morphogenesis with mesodermal fate acquisition

2020 ◽  
Author(s):  
Brian A. Kinney ◽  
Richard H. Row ◽  
Yu-Jung Tseng ◽  
Maxwell D. Weidmann ◽  
Holger Knaut ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Cell Fate ◽  
Epithelial To Mesenchymal Transition ◽  
Wnt Signaling Pathway ◽  
Mesoderm Induction ◽  
Cell Fate Specification ◽  
Canonical Wnt Signaling ◽  
Mesodermal Cell ◽  
Mesenchymal Transition ◽  
Canonical Wnt

AbstractAnimal embryogenesis requires a precise coordination between morphogenesis and cell fate specification. It is unclear if there are mechanisms that prevent uncoupling of these processes to ensure robust development. During mesoderm induction, mesodermal fate acquisition is tightly coordinated with the morphogenetic process of epithelial to mesenchymal transition (EMT). In zebrafish, cells exist transiently in a partial EMT state during mesoderm induction. Here we show that cells expressing the neural inducing transcription factor Sox2 are held in the partial EMT state, stopping them from completing the EMT and joining the mesodermal territory. This is critical for preventing ectopic neural tissue from forming. The mechanism involves specific interactions between Sox2 and the mesoderm inducing canonical Wnt signaling pathway. When Wnt signaling is inhibited in Sox2 expressing cells trapped in the partial EMT, cells are now able to exit into the mesodermal territory, but form an ectopic spinal cord instead of mesoderm. Our work identifies a critical developmental checkpoint that ensures that morphogenetic movements establishing the mesodermal germ layer are accompanied by robust mesodermal cell fate acquisition.

Xrel3/XrelA attenuates β-catenin-mediated transcription during mesoderm formation in Xenopus embryos

2011 ◽  
Vol 435 (1) ◽  
pp. 247-257 ◽  
Author(s):  
Mark W. L. Kennedy ◽  
Kenneth R. Kao
Keyword(s):  
Cell Fate ◽  
Target Genes ◽  
Marginal Zone ◽  
Ectopic Expression ◽  
Nuclear Factor Κb ◽  
Mesoderm Induction ◽  
Mesoderm Cell ◽  
Mesoderm Formation

In Xenopus laevis embryonic development, activation of the Wnt/β-catenin pathway promotes mesoderm cell fate determination via Xnr (Xenopus nodal-related) expression. We have demonstrated previously that Rel/NF-κB (nuclear factor κB) proteins expressed in presumptive ectoderm limit the activity of Xnrs to the marginal zone of embryos during mesoderm induction, which assists to distinguish mesoderm from ectoderm. The mechanism of this regulation, however, is unknown. In the present study, we investigated whether Rel/NF-κB proteins are able to modulate mesoderm formation by mediating Wnt/β-catenin signalling. We determined that ectopic expression of XrelA or Xrel3 in the dorsal marginal zone perturbed dorsal mesoderm formation by down-regulating multiple Wnt/β-catenin target genes including Xnr3, Xnr5 and Xnr6. Ventral co-expression of XrelA or Xrel3 with either wild-type β-catenin or constitutively active β-cateninS37A abrogated β-catenin-induced axis duplication and attenuated β-catenin-stimulated reporter transcription. Lastly, we provide evidence that Xrel3, but not XrelA, can interact with β-catenin without affecting the association of β-catenin with other transcriptional co-activators in vitro. Both Xrel3 and XrelA, however, prevented the accumulation, in nuclei, of exogenously expressed and endogenous β-catenin in vivo. These results suggest that Rel proteins are able to bind β-catenin and attenuate β-catenin-mediated transcription by nuclear exclusion.

scholarly journals Coordinate Control of Muscle Cell Survival by Distinct Insulin-like Growth Factor Activated Signaling Pathways

2000 ◽  
Vol 151 (6) ◽  
pp. 1131-1140 ◽  
Author(s):  
Margaret A. Lawlor ◽  
Peter Rotwein
Keyword(s):  
Growth Factors ◽  
Muscle Cell ◽  
Kinase Inhibitor ◽  
Ectopic Expression ◽  
Pi3 Kinase ◽  
Cellular Functions ◽  
Cyclin Dependent Kinase Inhibitor ◽  
Rapid Induction ◽  
Peptide Growth Factors ◽  
Igf I

Peptide growth factors control diverse cellular functions by regulating distinct signal transduction pathways. In cultured myoblasts, insulin-like growth factors (IGFs) stimulate differentiation and promote hypertrophy. IGFs also maintain muscle cell viability. We previously described C2 skeletal muscle lines lacking expression of IGF-II. These cells did not differentiate, but underwent progressive apoptotic death when incubated in differentiation medium. Viability could be sustained and differentiation enabled by IGF analogues that activated the IGF-I receptor; survival was dependent on stimulation of phosphatidylinositol 3-kinase (PI3-kinase). We now find that IGF action promotes myoblast survival through two distinguishable PI3-kinase–regulated pathways that culminate in expression of the cyclin-dependent kinase inhibitor, p21. Incubation with IGF-I or transfection with active PI3-kinase led to rapid induction of MyoD and p21, and forced expression of either protein maintained viability in the absence of growth factors. Ectopic expression of MyoD induced p21, and inhibition of p21 blocked MyoD-mediated survival, thus defining one PI3-kinase–dependent pathway as leading first to MyoD, and then to p21 and survival. Unexpectedly, loss of MyoD expression did not impede IGF-mediated survival, revealing a second pathway involving activation by PI3-kinase of Akt, and subsequent induction of p21. Since inhibition of p21 caused death even in the presence of IGF-I, these results establish a central role for p21 as a survival factor for muscle cells. Our observations also define a MyoD-independent pathway for regulating p21 in muscle, and demonstrate that distinct mechanisms help ensure appropriate expression of this key protein during differentiation.

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