Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Smad4 controls signaling robustness and morphogenesis by differentially contributing to the Nodal and BMP pathways

ABSTRACT: We explored the consequence of Smad4 gene loss for gene expression downstream BMP and Nodal signalling. To this end we performed RNA sequencing of WT and MZsmad4a mutants at mid-gastrulation.

ORGANISM(S): Danio rerio

PROVIDER: GSE162289 | GEO | 2021/08/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Smad4 controls signaling robustness and morphogenesis by differentially contributing to the Nodal and BMP pathways

Project description:The goal of this scRNA-seq study was to characterize the pseudo-spatial distribution of Nodal and BMP effectors (SMADs) expression prior to the onset of gastrulation

2021-04-11 | GSE164574 | GEO

Smad4 controls signaling robustness and morphogenesis by differentially contributing to the Nodal and BMP pathways

Project description:Smad4 controls signaling robustness and morphogenesis by differentially contributing to the Nodal and BMP pathways

| PRJNA681251 | ENA

Smad4 controls signaling robustness and morphogenesis by differentially contributing to the Nodal and BMP pathways

Project description:Smad4 controls signaling robustness and morphogenesis by differentially contributing to the Nodal and BMP pathways

| PRJNA691237 | ENA

Smad4 controls signaling robustness and morphogenesis by differentially contributing to the Nodal and BMP pathways.

Project description:The transcriptional effector SMAD4 is a core component of the TGF-β family signaling pathways. However, its role in vertebrate embryo development remains unresolved. To address this, we deleted Smad4 in zebrafish and investigated the consequences of this on signaling by the TGF-β family morphogens, BMPs and Nodal. We demonstrate that in the absence of Smad4, dorsal/ventral embryo patterning is disrupted due to the loss of BMP signaling. However, unexpectedly, Nodal signaling is maintained, but lacks robustness. This Smad4-independent Nodal signaling is sufficient for mesoderm specification, but not for optimal endoderm specification. Furthermore, using Optical Projection Tomography in combination with 3D embryo morphometry, we have generated a BMP morphospace and demonstrate that Smad4 mutants are morphologically indistinguishable from embryos in which BMP signaling has been genetically/pharmacologically perturbed. Smad4 is thus differentially required for signaling by different TGF-β family ligands, which has implications for diseases where Smad4 is mutated or deleted.

| S-EPMC8569018 | biostudies-literature

Smad4 and Trim33 dependend nodal/activin responsive genes in differentiated mouse ESCs

Project description:In differentiated mouse ESCs, most of the nodal/activin responsive genes are dependent on both Smad4 and Trim33, some are solely dependent on Smad4, and some are dependent on Trim33. Ebs at Day2.5 from WT, Smad4 null, and Trim33 knock-down ESCs, were treated with activin or SB 431542 for 2 h.

2012-01-09 | E-GEOD-32903 | biostudies-arrayexpress

Smad4 and Trim33 dependend nodal/activin responsive genes in differentiated mouse ESCs

2012-01-09 | GSE32903 | GEO

Transcription profiling of human mammary epithelial cell line MDA-MB-468 acking endogenous Smad4 nfected with either an adenovirus carrying GFP cDNA (control) or Smad4 cDNA (to restore the Smad4 activity in the cells). Cells were treated with TGF-b1 (0.5 ng/ml) or BMP-7 (300 ng/ml) for 2 or 12h

Project description:Identification of novel TGF-b1 and BMP-7-regulated genes in epithelial cells.<br> <br> Human mammary epithelial cell line MDA-MB-468 that is lacking endogenous Smad4 was infected with either an adenovirus carrying GFP cDNA (control) or Smad4 cDNA (to restore the Smad4 activity in the cells). Cells were treated with TGF-b1 (0.5 ng/ml) or BMP-7 (300 ng/ml) for 2 or 12h. Smad4-independent vs Smad4-dependent response was measured. Also response to both growth factors was compared.

2004-03-15 | E-MEXP-78 | biostudies-arrayexpress

HMCES counterbalances the transcriptional regulation of nodal/activin and BMP signaling in mESCs (RNA-Seq)

Project description:Despite the fundamental roles to cell fates determination in all metazoans, the mechanism by which the TGF-β family signaling is interpreted into spatial and temporal manner and multiple cell fates is still elusive. The cell context dependent function of TGF-β signaling largely relies on the transcriptional regulation centered by SMAD proteins. Here, we discovered that the DNA-repair related protein, HMCES contributes to early development by maintaining the nodal/activin or BMP signaling related transcriptome homeostasis. HMCES is a R-SMAD proteins binding partner that co-localizes with R-SMADs at active histone marks. However, HMCES chromatin occupancy is independent of nodal/activin or BMP signaling. Mechanically, HMCES exerts its transcriptional regulation role by counteracting R-SMAD proteins association with chromatin. In Xenopus embryo, hmces-KD causes dramatic development defects with altered left-right axis asymmetry along with increasing expression of lefty1. In sum, we disclosed the novel transcriptional regulatory function of HMCES integrated in TGF-β family signaling.

2022-09-14 | GSE186223 | GEO

HMCES counterbalances the transcriptional regulation of nodal/activin and BMP signaling in mESCs (ChIP-Seq)

2022-09-14 | GSE186222 | GEO

Population-level antagonism between FGF and BMP signaling steers mesoderm differentiation in embryonic stem cells

Project description:The mesodermal precursor populations for different internal organ systems are specified during gastrulation by the combined activity of extracellular signaling systems such as BMP, Wnt, Nodal, and FGF. The BMP, Wnt and Nodal signaling requirements for the differentiation of specific mesoderm subtypes in mammals have been mapped in detail, but which mesodermal cell types depend on FGF signaling is not precisely known. It is also not clear how FGF signaling modulates the activity of orthogonal signaling systems involved in mesoderm differentiation. Here, we address these questions by analyzing the effects of targeted signaling manipulations in differentiating stem cell populations with single cell resolution. We identify opposing functions of BMP and FGF, and map the boundary between FGF-dependent and -independent mesodermal lineages. Stimulation with exogenous FGF boosts the expression of endogenous Fgfs while repressing Bmp ligands. This intercellular positive autoregulation of FGF signaling coupled to the repression of BMP signaling may contribute to the specification of reproducible and coherent cohorts of cells with the same identity via a community effect, both in the embryo and in synthetic embryo-like systems.

2023-03-24 | GSE228061 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data