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Oligodendrocyte precursor differentiation and survival requires chromatin remodeling by Chd7 and Chd8

ABSTRACT: Oligodendrocyte precursor differentiation and survival requires chromatin remodeling by Chd7 and Chd8

PROVIDER: PRJNA479472 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7468350_1.fastq.gz	Fastqsanger.gz
	SRR7468350_2.fastq.gz	Fastqsanger.gz
	SRR7468360_1.fastq.gz	Fastqsanger.gz
	SRR7468360_2.fastq.gz	Fastqsanger.gz
	SRR7468370_1.fastq.gz	Fastqsanger.gz

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Oligodendrocyte precursor differentiation and survival requires chromatin remodeling by Chd7 and Chd8 [ATAC-seq]

Project description:Oligodendrocyte precursor cells (OPCs) constitute the main proliferative cells in the adult brain, and deregulation of OPC proliferation-differentiation balance results in either glioma formation or defective adaptive (re)myelination. OPC differentiation requires significant genetic reprogramming implicating chromatin remodeling. Here, we report on uncharacterized functions of the chromatin remodelers Chd7 and Chd8 in OPCs. Their OPC-chromatin-binding profile combined with transcriptome and open-chromatin analysis of Chd7-deleted OPCs, demonstrates that Chd7 controls OPC differentiation through chromatin-opening and transcriptional activation of key regulators such as Sox10, Nkx2.2 and Gpr17. Chd7 is however dispensable for oligodendrocyte stage progression, consistent with Chd8 compensatory function, as suggested by its chromatin binding profile. Furthermore, Chd7 protects non-proliferative OPCs from apoptosis by chromatin-closing and transcriptional repression of p53. Mutations in CHD7 and CHD8 are associated with developmental disorders, such as CHARGE syndrome and autism respectively, and our results offer new avenues to understand and modulate their functions in disease.

2018-08-29 | GSE116598 | GEO

Oligodendrocyte precursor differentiation and survival requires chromatin remodeling by Chd7 and Chd8 [RNA-seq]

Project description:Oligodendrocyte precursor cells (OPCs) constitute the main proliferative cells in the adult brain, and deregulation of OPC proliferation-differentiation balance results in either glioma formation or defective adaptive (re)myelination. OPC differentiation requires significant genetic reprogramming implicating chromatin remodeling. Mounting evidence indicates that chromatin remodelers play important roles during normal development and their mutations are associated with neurodevelopmental defects, with CHD7 haploinsuficiency being the cause of CHARGE syndrome and CHD8 being one of the strongest Autism Spectrum Disorder (ASD) high-risk associated genes. Here, we report on uncharacterized functions of the chromatin remodelers Chd7 and Chd8 in OPCs. Their OPC-chromatin-binding profile combined with transcriptome and chromatin accessibility analyses of Chd7-deleted OPCs, demonstrates that Chd7 protects non-proliferative OPCs from apoptosis by chromatin-closing and transcriptional repression of p53. Furthermore, Chd7 controls OPC differentiation through chromatin-opening and transcriptional activation of key regulators, including Sox10, Nkx2.2 and Gpr17. Chd7 is however dispensable for oligodendrocyte stage progression, consistent with Chd8 compensatory function, as suggested by their common chromatin binding profiles and genetic interaction. Finally, CHD7 and CHD8 bind in OPCs to a majority of ASD-risk associated genes, suggesting an implication of oligodendrocyte lineage cells in ASD neurological defects. Our results thus offer new avenues to understand and modulate the CHD7 and CHD8 functions in normal development and disease.

2018-08-29 | GSE116600 | GEO

Oligodendrocyte precursor differentiation and survival requires chromatin remodeling by Chd7 and Chd8 [ChIP-seq]

Project description:Oligodendrocyte precursor cells (OPCs) constitute the main proliferative cells in the adult brain, and deregulation of OPC proliferation-differentiation balance results in either glioma formation or defective adaptive (re)myelination. OPC differentiation requires significant genetic reprogramming implicating chromatin remodeling. Mounting evidence indicates that chromatin remodelers play important roles during normal development and their mutations are associated with neurodevelopmental defects, with CHD7 haploinsuficiency being the cause of CHARGE syndrome and CHD8 being one of the strongest Autism Spectrum Disorder (ASD) high-risk associated genes. Here, we report on uncharacterized functions of the chromatin remodelers Chd7 and Chd8 in OPCs. Their OPC-chromatin-binding profile combined with transcriptome and chromatin accessibility analyses of Chd7-deleted OPCs, demonstrates that Chd7 protects non-proliferative OPCs from apoptosis by chromatin-closing and transcriptional repression of p53. Furthermore, Chd7 controls OPC differentiation through chromatin-opening and transcriptional activation of key regulators, including Sox10, Nkx2.2 and Gpr17. Chd7 is however dispensable for oligodendrocyte stage progression, consistent with Chd8 compensatory function, as suggested by their common chromatin binding profiles and genetic interaction. Finally, CHD7 and CHD8 bind in OPCs to a majority of ASD-risk associated genes, suggesting an implication of oligodendrocyte lineage cells in ASD neurological defects. Our results thus offer new avenues to understand and modulate the CHD7 and CHD8 functions in normal development and disease.

2018-08-29 | GSE116599 | GEO

Oligodendrocyte precursor differentiation and survival requires chromatin remodeling by Chd7 and Chd8 [RNA-seq]

Project description:Oligodendrocyte precursor differentiation and survival requires chromatin remodeling by Chd7 and Chd8 [RNA-seq]

| PRJNA479476 | ENA

Oligodendrocyte precursor differentiation and survival requires chromatin remodeling by Chd7 and Chd8 [ChIP-seq]

Project description:Oligodendrocyte precursor differentiation and survival requires chromatin remodeling by Chd7 and Chd8 [ChIP-seq]

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Oligodendrocyte precursor differentiation and survival requires chromatin remodeling by Chd7 and Chd8 [ATAC-seq]

Project description:Oligodendrocyte precursor differentiation and survival requires chromatin remodeling by Chd7 and Chd8 [ATAC-seq]

| PRJNA479474 | ENA

Expression profiles in Chd7 knockdown oligodendrocyte precursor cells

Project description:Oligodendrocytes are generated from oligodendrocyte precursor cells (OPCs). Chd7 is ATP-dependent chromatin-remodeling enzyme. We performed microarray analysis to examine changes in gene expression between control and Chd7 knockdown OPCs. Results provide insight into the function of Chd7 in oligodendrocyte development.

2018-03-01 | GSE95347 | GEO

Oligodendrocyte precursor survival and differentiation requires chromatin remodeling by Chd7 and Chd8.

Project description:Oligodendrocyte precursor cells (OPCs) constitute the main proliferative cells in the adult brain, and deregulation of OPC proliferation-differentiation balance results in either glioma formation or defective adaptive (re)myelination. OPC differentiation requires significant genetic reprogramming, implicating chromatin remodeling. Mounting evidence indicates that chromatin remodelers play important roles during normal development and their mutations are associated with neurodevelopmental defects, with CHD7 haploinsuficiency being the cause of CHARGE syndrome and CHD8 being one of the strongest autism spectrum disorder (ASD) high-risk-associated genes. Herein, we report on uncharacterized functions of the chromatin remodelers Chd7 and Chd8 in OPCs. Their OPC-chromatin binding profile, combined with transcriptome and chromatin accessibility analyses of Chd7-deleted OPCs, demonstrates that Chd7 protects nonproliferative OPCs from apoptosis by chromatin closing and transcriptional repression of p53 Furthermore, Chd7 controls OPC differentiation through chromatin opening and transcriptional activation of key regulators, including Sox10, Nkx2.2, and Gpr17 However, Chd7 is dispensable for oligodendrocyte stage progression, consistent with Chd8 compensatory function, as suggested by their common chromatin-binding profiles and genetic interaction. Finally, CHD7 and CHD8 bind in OPCs to a majority of ASD risk-associated genes, suggesting an implication of oligodendrocyte lineage cells in ASD neurological defects. Our results thus offer new avenues to understand and modulate the CHD7 and CHD8 functions in normal development and disease.

| S-EPMC6126750 | biostudies-literature

Oligodendrocyte precursor differentiation and survival requires chromatin remodeling by Chd7 and Chd8

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

2018-08-29 | GSE116601 | GEO

Investigation of Oligodendrocyte Precursor Cell Differentiation by Quantitative Proteomics

Project description:Oligodendrocytes, the myelinating cells of the central nervous system, are essential for correct brain function. They originate from oligodendrocyte precursor cells (OPCs) through a differentiation process which is only incompletely understood and impaired in a variety of demyelinating diseases. Better knowledge of this differentiation holds the promise to develop novel therapies for these disorders. We investigated the differentiation of rat oligodendrocyte precursor cells to oligodendrocytes in vitro. After confirmation of differentiation by immunohistochemical analysis using cell type-specific marker proteins, we conducted a quantitative proteomics study using tandem mass tags (TMT). We investigated four time points of differentiation covering early, intermediate, and late stages. Data analysis was perfomed using Mascot and Maxquant.

2019-06-21 | PXD012544 | Pride

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