Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression changes in mouse oligodendrocytes after deletion of the Ep400 chromatin remodeler

ABSTRACT: Expression changes in mouse oligodendrocytes after deletion of the Ep400 chromatin remodeler

PROVIDER: PRJNA488235 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7761300.fastq.gz	Fastqsanger.gz
	SRR7761301.fastq.gz	Fastqsanger.gz
	SRR7761297.fastq.gz	Fastqsanger.gz
	SRR7761298.fastq.gz	Fastqsanger.gz
	SRR7761299.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Expression changes in mouse oligodendrocytes after deletion of the Ep400 chromatin remodeler

Project description:To address the role of INO80/SWR-type remodeling complexes, we deleted Ep400 at defined times of mouse oligodendrocyte development. Whereas oligodendrocyte precursors are specified and develop normally without Ep400, terminal differentiation is dramatically impaired resulting in hypomyelination. RNA-Seq studies were performed on cultured and FACS sorted control and Ep400-deficient mouse oligodendrocytes to analyze changes in gene expression. These revealed that genes associated with the myelination program and with response to DNA damage are altered in Ep400-deficient oligodendrocytes.

2019-05-17 | GSE119127 | GEO

Expression changes in early postnatal mouse sciatic nerve after Schwann cell-specific deletion of the Ep400 chromatin remodeler

Project description:To address the role of INO80/SWR-type remodeling complexes, we deleted Ep400 in developing Schwann cells. Ep400 becomes important for proper Schwann cell development at differentiation. Its absence in Schwann cells leads to a peripheral neuropathy. RNA-Seq studies were performed on sciatic nerve from control mice and mice with a Schwann cell-specific deletion of Ep400 to analyze changes in gene expression. These revealed substantial changes in the expression of genes associated with immune and inflammatory response, myelination-associated lipid metabolism and developmental regulatory genes whose occurrence and action is normally limited to earlier stages of development.

2019-04-18 | GSE119132 | GEO

Expression changes in early postnatal mouse sciatic nerve after Schwann cell-specific deletion of the Ep400 chromatin remodeler

Project description:Expression changes in early postnatal mouse sciatic nerve after Schwann cell-specific deletion of the Ep400 chromatin remodeler

| PRJNA488240 | ENA

Altered genomic occupancy of H2A.Z in early postnatal mouse sciatic nerve after Schwann cell-specific deletion of the Ep400 chromatin remodeler

Project description:To address the role of INO80/SWR-type remodeling complexes, we deleted Ep400 in developing Schwann cells. Ep400 is involved in exchanging H2A-containing standard with H2A.Z-containing nucleosomes. Ep400 becomes important for proper Schwann cell development at differentiation. Its absence in Schwann cells leads to a peripheral neuropathy. ChIP-Seq studies were performed with H2A.Z-specific antibodies on sciatic nerve from control mice and mice with a Schwann cell-specific deletion of Ep400 to determine the genomic occupancy of this histone variant. One group of genes with strongly altered H2A.Z occupancy around the transcriptional start site consisted of developmental regulatory genes whose occurrence and action is normally limited to earlier stages of development.

2019-04-18 | GSE119194 | GEO

Altered genomic occupancy of H2A.Z in early postnatal mouse sciatic nerve after Schwann cell-specific deletion of the Ep400 chromatin remodeler

Project description:Altered genomic occupancy of H2A.Z in early postnatal mouse sciatic nerve after Schwann cell-specific deletion of the Ep400 chromatin remodeler

| PRJNA488439 | ENA

Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler [RNA-Seq]

Project description:Alu retrotransposons, forming the largest family of mobile DNA elements in the human genome, have recently come to attention as a potential source of regulatory novelties, most notably by participating in enhancer function. Even though Alu transcription by RNA polymerase III is subjected to tight epigenetic silencing, their bulk expression has long been known to increase in response to various types of stress, including viral infection. Here we show that, in primary human fibroblasts, adenovirus small e1a triggered derepression of hundreds of individual Alus, by promoting TFIIIB recruitment by Alu-bound TFIIIC. Epigenome profiling revealed an e1a-induced decrease of H3K27 acetylation and increase of H3K4 monomethylation at derepressed Alus, making them resemble poised enhancers. The enhancer nature of e1a-targeted Alus was confirmed by the enrichment, in their upstream regions, of the EP300/CBP acetyltransferase and of the YAP1 and FOS transcription factors. The physical interaction of e1a with the chromatin remodeler EP400 turned out to be critical for Alu derepression, and upstream enrichment of EP400 was found to commonly demarcate expression-prone Alus. Our data suggest that e1a targets a subset of enhancer Alus whose transcriptional activation, mediated by e1a-EP400 interaction, may participate in the manipulation of enhancer activity by adenovirus.

2024-03-31 | GSE208716 | GEO

Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler [ChIP-Seq]

2024-03-31 | GSE208685 | GEO

EP400 Deposits H3.3 into Promoters and Enhancers During Gene Activation

Project description:Purpose: We wanted to know how histone variants H3.3 and H2AZ are deposited into genes and enhancers during gene activation Methods: U2OS cells were harvested at 70% confluency with formaldehyde crosslinking for ChIP-seq without crosslinking for RNA-seq. ChIP DNA were purified through standard chromatin immunoprecipitation using an Pol II, MED26, EP400, H3.3, H2AZ, H3k4me1 and K3K18ac antibodies. Libraries were prepared with a KAPA LTP kit and sequenced using the Illumina HiSeq 2000 platform. Total RNA was extracted with Trizol, digested with DNaseI and further purified by acid phenol. Libraries were prepared with Illumina TruSeq RNA Sample Prep Kits v2 and were sequenced on Illumina HiSeq 2000. Conclusion: Our biochemical and genomics (ChIP-Seq and mRNA-Seq) data show that EP400 contributes to H3.3 deposition in significantly with less of an effect on H2AZ in both genes and enhancers Enrichment of EP400, Pol II, MED26, Histone varinat H3.3 and H2AZ, and enhancers marks H3K4me1 and H3K18ac in either Mock and/or EP400 knockdown conditions on chromatin were generated by ChIP-Seq. mRNA profiles under Mock siRNA or EP400siRNA were generated by deep sequencing, using Illumina HiSeq 2000.

2015-12-18 | E-GEOD-73742 | biostudies-arrayexpress

CSN5 deletion in oligodendrocytes causes senescence-induced inflammation and neurodegeneration

Project description:Oligodendrocytes are the primary target of demyelinating disorders in the CNS, which may evolve in neurodegeneration. DNA damage and oxidative stress are considered key pathogenic events, but the underlying molecular mechanisms remain unclear. Moreover, comprehensive animal models are lacking or do not fully recapitulate human diseases, complicating the path to effective treatments. Here we report that mice with cell autonomous deletion of the COP9 signalosome component CSN5 (Jab1) in oligodendrocytes develop DNA damage and defective DNA repair in myelinating glial cells. Interestingly, oligodendrocytes lacking Jab1 expression undergo a senescence-like phenotype that fosters chronic inflammation and oxidative stress. These mutants develop progressive CNS demyelination, microglia inflammation and neurodegeneration, with severe motor deficits and premature death. Notably, blocking microglia inflammation did not prevent neurodegeneration; whereas, deletion of p21CIP1 but not p16INK4a pathway ameliorated the disease. We suggest that senescence is key to sustaining neurodegeneration in demyelinating disorders and might represent a new potential therapeutic target.

2022-02-09 | GSE184573 | GEO

Age-dependent changes in translational expression of oligodendrocytes

Project description:Age-dependent changes in translational expression of oligodendrocytes

| PRJEB19341 | ENA