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Snail regulates MyoD binding-site occupancy to direct enhancer switching and differentiation-specific transcription in myogenesis

ABSTRACT: Snail regulates MyoD binding-site occupancy to direct enhancer switching and differentiation-specific transcription in myogenesis

PROVIDER: PRJNA132093 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR070046.fastq.gz	Fastqsanger.gz
	SRR070047.fastq.gz	Fastqsanger.gz
	SRR070048.fastq.gz	Fastqsanger.gz
	SRR070049.fastq.gz	Fastqsanger.gz
	SRR070050.fastq.gz	Fastqsanger.gz

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Snail regulates MyoD binding-site occupancy to direct enhancer switching and differentiation-specific transcription in myogenesis

Project description:This SuperSeries is composed of the following subset Series: GSE24811: Time Series of Mouse skeletal muscle cell differentiation GSE24852: ChIP-Seq of MyoD, Myf5, Snai1, HDAC1, HDAC2, E47 and empty vector controls in mouse skeletal myoblasts or myotubes GSE38236: RNA-Seq of si-Snai1, si-Snai2, si-Snai1/2 and si-Scrambled treated myoblasts Refer to individual Series

2012-07-04 | E-GEOD-24904 | biostudies-arrayexpress

Snail regulates MyoD binding-site occupancy to direct enhancer switching and differentiation-specific transcription in myogenesis.

Project description:In skeletal myogenesis, the transcription factor MyoD activates distinct transcriptional programs in progenitors compared to terminally differentiated cells. Using ChIP-Seq and gene expression analyses, we show that in primary myoblasts, Snail-HDAC1/2 repressive complex binds and excludes MyoD from its targets. Notably, Snail binds E box motifs that are G/C rich in their central dinucleotides, and such sites are almost exclusively associated with genes expressed during differentiation. By contrast, Snail does not bind the A/T-rich E boxes associated with MyoD targets in myoblasts. Thus, Snai1-HDAC1/2 prevent MyoD occupancy on differentiation-specific regulatory elements, and the change from Snail to MyoD binding often results in enhancer switching during differentiation. Furthermore, we show that a regulatory network involving myogenic regulatory factors (MRFs), Snai1/2, miR-30a, and miR-206 acts as a molecular switch that controls entry into myogenic differentiation. Together, these results reveal a regulatory paradigm that directs distinct gene expression programs in progenitors versus terminally differentiated cells.

| S-EPMC4580277 | biostudies-literature

ChIP-Seq of Myf5, MyoD, Snai1, HDAC1, HDAC2, E47 and empty vector controls in mouse skeletal myoblasts or myotubes

Project description:In skeletal myogenesis, the transcription factor MyoD activates distinct transcriptional programs in progenitors compared to terminally differentiated cells. Using ChIP-seq and gene expression analyses, we show that in primary myoblasts, Snail-HDAC1/2 repressive complex bind and exclude MyoD from its targets. Notably, Snail binds E-box motifs that are G/C-rich in their central dinucleotides, and such sites are almost exclusively associated with genes expressed during differentiation. By contrast, Snail does not bind the A/T-rich E-boxes associated with MyoD targets in myoblasts. Thus, Snai1-HDAC1/2 prevents MyoD occupancy on differentiation-specific regulatory elements and the change from Snail- to MyoD-binding often results in enhancer switching during differentiation. Furthermore, we show that a regulatory network involving Myogenic Regulatory Factors (MRFs), Snail/2, miR-30a and miR-206 acts as a molecular switch that controls entry into myogenic differentiation. Together, these results reveal a regulatory paradigm that directs distinct gene expression programs in progenitors versus terminally differentiated cells. Genome wide binding sites of various transcription factors and chromatin modifiers in muscle cells

2012-07-04 | E-GEOD-24852 | biostudies-arrayexpress

ChIP-Seq of Myf5, MyoD, Snai1, HDAC1, HDAC2, E47 and empty vector controls in mouse skeletal myoblasts or myotubes

Project description:In skeletal myogenesis, the transcription factor MyoD activates distinct transcriptional programs in progenitors compared to terminally differentiated cells. Using ChIP-seq and gene expression analyses, we show that in primary myoblasts, Snail-HDAC1/2 repressive complex bind and exclude MyoD from its targets. Notably, Snail binds E-box motifs that are G/C-rich in their central dinucleotides, and such sites are almost exclusively associated with genes expressed during differentiation. By contrast, Snail does not bind the A/T-rich E-boxes associated with MyoD targets in myoblasts. Thus, Snai1-HDAC1/2 prevents MyoD occupancy on differentiation-specific regulatory elements and the change from Snail- to MyoD-binding often results in enhancer switching during differentiation. Furthermore, we show that a regulatory network involving Myogenic Regulatory Factors (MRFs), Snail/2, miR-30a and miR-206 acts as a molecular switch that controls entry into myogenic differentiation. Together, these results reveal a regulatory paradigm that directs distinct gene expression programs in progenitors versus terminally differentiated cells.

2012-07-05 | GSE24852 | GEO

Snail regulates MyoD binding-site occupancy to direct enhancer switching and differentiation-specific transcription in myogenesis

Project description:This SuperSeries is composed of the SubSeries listed below.

2012-07-05 | GSE24904 | GEO

Myogenesis MyoD

Project description:The transcription factor MyoD can coax na?e fibroblasts or otherwise committed cells to adopt the skeletal muscle phenotype by activating the muscle gene expression program. Activation of muscle gene expression occurs in quantal steps with not all the target genes of MyoD being activated at the same time. Some genes are induced in the initial phases, others at later stages despite the fact that MyoD is present throughout the differentiation process. MyoD is post-translationally modified by phosphorylation, ubiquitination, and acetylation. Here, we have employed a model system in which MyoD and its non-acetylatable version were inducibly expressed in mouse embryonic fibroblasts derived from mice to investigate how MyoD acetylation may contribute to differential gene activation. Keywords: Time-Series

2006-12-13 | GSE6487 | GEO

Conversion of MyoD to a neurogenic factor: binding site specificity determines lineage [ChIP-seq]

Project description:MyoD and NeuroD2 are master regulators of myogenesis and neurogenesis and bind to a "shared" E-box sequence (CAGCTG) and a "private" sequence (CAGGTG or CAGATG, respectively). To determine whether private-site recognition is sufficient to confer lineage-specification, we generated a MyoD-mutant with the DNA binding specificity of NeuroD2. Our results demonstrate that redirecting MyoD binding from MyoD-private sites to NeuroD2-private sites, despite preserved binding to the MyoD/NeuroD2-shared sites, is sufficient to change MyoD from a master regulator of myogenesis to a master regulator of neurogenesis.

2015-07-31 | GSE64626 | GEO

Conversion of MyoD to a neurogenic factor: binding site specificity determines lineage [RNA-seq]

2015-07-31 | GSE64622 | GEO

Conversion of MyoD to a neurogenic factor: binding site specificity determines lineage [RNA-seq]

2015-07-31 | E-GEOD-64622 | biostudies-arrayexpress

Conversion of MyoD to a neurogenic factor: binding site specificity determines lineage [ChIP-seq]

2015-07-31 | E-GEOD-64626 | biostudies-arrayexpress