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STAG2 promotes the myelination transcriptional program in oligodendrocytes [RNA-seq]

ABSTRACT: STAG2 promotes the myelination transcriptional program in oligodendrocytes [RNA-seq]

PROVIDER: PRJNA776652 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16652530_1.fastq.gz	Fastqsanger.gz
	SRR16652530_2.fastq.gz	Fastqsanger.gz
	SRR16652531_1.fastq.gz	Fastqsanger.gz
	SRR16652531_2.fastq.gz	Fastqsanger.gz
	SRR16652532_1.fastq.gz	Fastqsanger.gz

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STAG2 promotes the myelination transcriptional program in oligodendrocytes

Project description:STAG2 promotes the myelination transcriptional program in oligodendrocytes

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STAG2 promotes the myelination transcriptional program in oligodendrocytes [scRNA-seq]

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STAG2 promotes the myelination transcriptional program in oligodendrocytes [Hi-C]

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STAG2 promotes the myelination transcriptional program in oligodendrocytes [ChIP-seq]

Project description:STAG2 promotes the myelination transcriptional program in oligodendrocytes [ChIP-seq]

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STAG2 promotes the myelination transcriptional program in oligodendrocytes [ChIP-seq]

Project description:Cohesin folds chromosomes via DNA loop extrusion. Cohesin-mediated chromosome loops regulate transcription by shaping long-range enhancer-promoter interactions, among other mechanisms. Mutations of cohesin subunits and regulators cause human developmental diseases termed cohesinopathy. Vertebrate cohesin consists of SMC1, SMC3, RAD21, and either STAG1 or STAG2. To probe the physiological functions of cohesin, we created conditional knockout (cKO) mice with Stag2 deleted in the nervous system. Stag2 cKO mice exhibit growth retardation, neurological defects, and premature death, in part due to insufficient myelination of nerve fibers. Stag2 cKO oligodendrocytes exhibit delayed maturation and downregulation of myelinationrelated genes. Stag2 loss reduces promoter-anchored loops at downregulated genes in oligodendrocytes. Thus, STAG2-cohesin generates promoter-anchored loops at myelinationpromoting genes to facilitate their transcription. Our study implicates defective myelination as a contributing factor to cohesinopathy and establishes oligodendrocytes as a relevant cell type to explore the mechanisms by which cohesin regulates transcription.

2022-08-23 | GSE186891 | GEO

STAG2 promotes the myelination transcriptional program in oligodendrocytes [RNA-seq]

2022-08-23 | GSE186890 | GEO

STAG2 promotes the myelination transcriptional program in oligodendrocytes [Hi-C]

2022-08-23 | GSE186893 | GEO

STAG2 promotes the myelination transcriptional program in oligodendrocytes [scRNA-seq]

2022-08-23 | GSE186892 | GEO

STAG2 promotes the myelination transcriptional program in oligodendrocytes.

Project description:Cohesin folds chromosomes via DNA loop extrusion. Cohesin-mediated chromosome loops regulate transcription by shaping long-range enhancer-promoter interactions, among other mechanisms. Mutations of cohesin subunits and regulators cause human developmental diseases termed cohesinopathy. Vertebrate cohesin consists of SMC1, SMC3, RAD21, and either STAG1 or STAG2. To probe the physiological functions of cohesin, we created conditional knockout (cKO) mice with Stag2 deleted in the nervous system. Stag2 cKO mice exhibit growth retardation, neurological defects, and premature death, in part due to insufficient myelination of nerve fibers. Stag2 cKO oligodendrocytes exhibit delayed maturation and downregulation of myelination-related genes. Stag2 loss reduces promoter-anchored loops at downregulated genes in oligodendrocytes. Thus, STAG2-cohesin generates promoter-anchored loops at myelination-promoting genes to facilitate their transcription. Our study implicates defective myelination as a contributing factor to cohesinopathy and establishes oligodendrocytes as a relevant cell type to explore the mechanisms by which cohesin regulates transcription.

| S-EPMC9439679 | biostudies-literature

STAG2 promotes the myelination transcriptional program in oligodendrocytes

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

2022-08-23 | GSE186894 | GEO