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TGF-β signaling controls neural crest developmental plasticity via SMAD2/3 [CUT&RUN]

ABSTRACT: TGF-β signaling controls neural crest developmental plasticity via SMAD2/3 [CUT&RUN]

PROVIDER: PRJNA733779 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14690743_1.fastq.gz	Fastqsanger.gz
	SRR14690743_2.fastq.gz	Fastqsanger.gz
	SRR14690744_1.fastq.gz	Fastqsanger.gz
	SRR14690744_2.fastq.gz	Fastqsanger.gz
	SRR14690745_1.fastq.gz	Fastqsanger.gz

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TGF-β signaling controls neural crest developmental plasticity via SMAD2/3

Project description:TGF-β signaling controls neural crest developmental plasticity via SMAD2/3

| PRJNA733778 | ENA

TGF-β signaling controls neural crest developmental plasticity via SMAD2/3 [CUT&RUN]

Project description:The neural crest is a highly plastic stem cell population that represents a notable exception to the germ layer theory. Despite being of ectodermal origin, these cells can differentiate into skeletal derivatives like cartilage and bone, tissues that are typically formed by mesoderm. The inductive program that endows the neural crest with these unique properties is still poorly understood. Here, we report that Smad2/3-mediated TGFβ signaling endows cranial neural crest cells with enhanced developmental potential. Our results show that TGFβ signaling modulates neural crest axial identity and directly activates the gene circuits that support skeletal differentiation. Cooperation between TGFβ and low levels of WNT-signaling in the embryonic head activates cranial-specific cis-regulatory elements of anterior genes. Activation of the TGFβ pathway allowed reprogramming of trunk neural crest cells to adopt an anterior identity and led to the development of an improved protocol for the generation of human cranial neural crest cells. Our findings indicate TGFβ signaling is required for the specification of cranial neural crest cells, endowing them with the potential to give rise to the craniofacial skeleton.

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TGF-β signaling controls neural crest developmental plasticity via SMAD2/3 [ATAC-seq]

Project description:TGF-β signaling controls neural crest developmental plasticity via SMAD2/3 [ATAC-seq]

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TGF-β signaling controls neural crest developmental plasticity via SMAD2/3 [TGF-β KD RNA-seq]

Project description:TGF-β signaling controls neural crest developmental plasticity via SMAD2/3 [TGF-β KD RNA-seq]

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TGF-β signaling controls neural crest developmental plasticity via SMAD2/3 [hiNCC RNA-seq]

Project description:TGF-β signaling controls neural crest developmental plasticity via SMAD2/3 [hiNCC RNA-seq]

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TGF-β signaling controls neural crest developmental plasticity via SMAD2/3 [ATAC-seq]

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The phosphorylation of the Smad2/3 linker region by Nemo-like kinase regulates TGF-β signaling

Project description:Smad2 and Smad3 (Smad2/3) primarily mediates the transforming growth factor-β (TGF-β) signaling that drives cell proliferation, differentiation, and migration. The dynamics of the Smad2/3 phosphorylation provides the key mechanism for regulating the TGF-β signaling pathway. Here we identified NLK as a novel regulator of TGF-β signaling pathway via modulating the phosphorylation of Smad2/3 in the linker region.

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TGF-beta-induced gene expression data and Smad2/3 binding sites of HaCaT keratinocytes

Project description:Smad2/3 are transcription factors that engage in TGF-beta-induced transcription. Here we analyzed the effect of identified Smad2/3 binding sites to transcription. We used expression microarrays to compare the Smad2/3 binding sites identified by ChIP-chip to TGF-beta-induced gene expressions. Keywords: time course We also examined the effect of either ETS1/TFAP2A/SMAD2/SMAD3 siRNAs on TGF-beta-induced gene expression change.

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