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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

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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

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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.

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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

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