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

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

PROVIDER: PRJNA691237 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13402902.fastq.gz	Fastqsanger.gz
	SRR13402903.fastq.gz	Fastqsanger.gz
	SRR13402904.fastq.gz	Fastqsanger.gz
	SRR13402905.fastq.gz	Fastqsanger.gz
	SRR13402906.fastq.gz	Fastqsanger.gz

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

Project description: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.

2021-08-31 | GSE162289 | 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

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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: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.

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

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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.

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High affinity enhancer promoter interactions can bypass strong CTCF/cohesin-mediated insulation contributing to phenotypic robustness

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Chromatin and Transcriptional Signatures for Nodal Signaling During Endoderm Formation in hESCs

Project description:To elucidate the Nodal transcriptional network that governs endoderm formation, we used ChIP-Seq to identify genomic targets for SMAD2/3, SMAD3, SMAD4, FOXH1 and the active and repressive chromatin marks, H3K4me3 and H3K27me3, in human embryonic stem cells (hESCs) and derived endoderm. We demonstrate that while SMAD2/3, SMAD4 and FOXH1 target binding is highly dynamic, there is an optimal signature for driving endoderm commitment. Initially, this signature is marked by both H3K4me3 and H3K27me3 as a very broad bivalent domain in hESCs. Within the first 24 hours, at a few select promoters, SMAD2/3 accumulation coincides with H3K27me3 depletion so that these loci become selectively monovalent marked only by H3K4me3. The correlation between SMAD2/3 binding, monovalent formation and transcriptional activation suggests a mechanism by which SMAD proteins coordinate with chromatin at critical promoters to drive endoderm specification. Examination of 2 different histone modifications and 4 different transcription factor associations in 2 cell types. For transcription factor analysis, three biological replicate ChIPs were pooled from each antibody, as well as input controls, for both hESCs and derived endoderm. For histone modifications, two biological replicates for H3K4me3 and three for H3K27me3 were used.

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Tissue-intrinsic beta-catenin signals antagonize Nodal-driven anterior visceral endoderm differentiation

Project description:The anterior-posterior axis of the mammalian embryo is laid down by the anterior visceral endoderm (AVE), an extraembryonic signaling center that is specified within the visceral endoderm. Current models posit that AVE differentiation is promoted globally by epiblast-derived Nodal signals, and spatially restricted by a BMP gradient established by the extraembryonic ectoderm. Here, we report spatially restricted AVE differentiation in bilayered embryo-like aggregates made from mouse embryonic stem cells that lack an extraembryonic ectoderm. Notably, clusters of AVE cells also form in pure visceral endoderm cultures upon activation of Nodal signaling, indicating that tissue-intrinsic factors can restrict AVE differentiation. We identify β-catenin activity as a tissue-intrinsic factor that antagonizes AVE-inducing Nodal signals. Together, our results show how an AVE-like population can arise through interactions between epiblast and visceral endoderm alone. This mechanism may be a flexible solution for axis patterning in a wide range of embryo geometries, and provide robustness to axis patterning when coupled with signal gradients.

2023-05-19 | GSE198780 | GEO

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