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

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

PROVIDER: PRJNA488439 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7765380.fastq.gz	Fastqsanger.gz
	SRR7765390.fastq.gz	Fastqsanger.gz
	SRR7765381.fastq.gz	Fastqsanger.gz
	SRR7765391.fastq.gz	Fastqsanger.gz
	SRR7765382.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

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

Single-cell RNA-seq reveals the difference between Schwann cells in dorsal root ganglion and sciatic nerve

Project description:Schwann cells are important glial cells in peripheral nervous system. In this study, we performed single cell RNA-sequencing (scRNA-seq) analysis of Schwann cells exist in both dorsal root ganglion(DRG) and sciatic nerve.We categorized DRG and sciatic nerve Schwann cells into different subtypes,and found common subtypes and different subtypes.In addition, we discovered the proliferation and migration ability of Schwann cells were distinct in different tissues.Our current study revealed the distinctive characteristics of Schwann cells in DRG and sciatic nerve.

2023-03-26 | GSE147615 | GEO

Expression data of sciatic nerves from mice with Schwann-cell specific Sip1 deletion compared to control mice.

Project description:Schwann cell maturation is tightly controlled by a set of transcriptional regulators. We have deleted the zinc-finger transcription factor Sip1 specifically from immature Schwann cells and observed a dramatic developmental delay. In an attempt to define the developmental stage of Sip1-deficient Schwann cells, we performed microarray analysis of Schwann cell-specific mutants compared to controls at the age of 25 days (P25). Sciatic nerves of 3 mutant mice and 3 corresponding controls were isolated at the age of 25 days.

2016-06-13 | E-GEOD-76027 | biostudies-arrayexpress

Nucleic acid sequence contributes to remodeler-mediated targeting of histone H2A.Z

Project description:The variant histone H2A.Z is inserted into nucleosomes immediately downstream of promoters and is important for transcription. The site-specific deposition of H2A.Z is catalyzed by SWR, a conserved chromatin remodeler with affinity for promoter-proximal nucleosome depleted regions (NDRs) and histone acetylation. By comparing the genomic distribution of H2A.Z in wild-type and SWR-deficient cells, we found that SWR is also responsible for depositing H2A.Z at thousands of non-canonical sites not directly linked to NDRs or histone acetylation. To understand the targeting mechanism of H2A.Z, we presented SWR with a library of nucleosomes isolated from yeast and characterized those preferred by SWR. We found that SWR prefers nucleosomes associated with intergenic over coding regions, especially when polyadenine tracks are present. Insertion of polyadenine sequences into recombinant nucleosomes near the H2A-H2B binding site stimulated the H2A.Z insertion activity of SWR. Therefore, the genome is encoded with information contributing to remodeler-mediated targeting of H2A.Z.

2024-01-13 | GSE252824 | GEO

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 mouse oligodendrocytes after deletion of the Ep400 chromatin remodeler

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

| PRJNA488235 | ENA

Functions of HDAC1 and HDAC2 in Schwann cells during postnatal

Project description:The aim of our study is to determine the functions of histone deacetylases (HDACs) 1 and 2 in Schwann cells during postnatal development of the peripheral nervous system (PNS). Schwann cells are the myelinating glial cells of the PNS. At birth, mouse sciatic nerves mature in 2 subsequent phases: 1/ big caliber axons get sorted into a 1 to 1 relationship with Schwann cells, 2/ Schwann cells build a myelin sheath around sorted axons. In mice where both HDAC1 & HDAC2 have been specifically knocked out in Schwann cells, both phases are impaired. HDACs are chromatin remodeling enzymes, they can thus alter gene expression directly. We want to identify which genes controlled by HDAC1 and HDAC2 in Schwann cells are necessary for the maturation of sciatic nerves. Because HDAC1 and HDAC2 can compensate for each other loss to some extend, we will first analyze changes of gene expression in HDAC1/HDAC2 double KO animals. We expect to gain critical insights into the molecular mechanisms controlling Schwann cell differentiation and myelination. This knowledge is of key importance for the success of regenerative medicine in peripheral neuropathies, nerve tumors, and transplantation paradigms in non-regenerative CNS lesions and in large PNS injuries. 3 double knockout mutants for HDAC1 and HDAC2 and 3 control littermates were analyzed. Tissues analyzed: sciatic nerves of 2 day-old mouse pups

2011-02-25 | E-GEOD-27451 | biostudies-arrayexpress

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

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