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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: PRJNA681251 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13160658_1.fastq.gz	Fastqsanger.gz
	SRR13160658_2.fastq.gz	Fastqsanger.gz
	SRR13160659_1.fastq.gz	Fastqsanger.gz
	SRR13160659_2.fastq.gz	Fastqsanger.gz
	SRR13160660_1.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

| PRJNA691237 | ENA

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.

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

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Nodal

Project description:Mus musculus Nodal, nodal [Source:MGI Symbol;Acc:MGI:97359], is differentially expressed in 30 experiment(s);

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