Ontology highlight
ABSTRACT:
PROVIDER: PRJNA213557 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1029631.fastq.gz | Fastqsanger.gz | |||
| SRR1029632.fastq.gz | Fastqsanger.gz | |||
| SRR1032220.fastq.gz | Fastqsanger.gz | |||
| SRR1032221.fastq.gz | Fastqsanger.gz | |||
| SRR935067.fastq.gz | Fastqsanger.gz |
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Project description:H2A.B is a unique histone H2A variant that shares only 40 ~ 50 % sequence identity with canonical H2A. It has only been identified in mammals and has quickly evolved with remarkable sequence diversity among different species. H2A.B is ubiquitously expressed in most cells and tissues. It is mainly deposited in gene body region. The localization of H2A.B is associated with methylated CpG islands in mouse ES cells. H2A.B facilitates transcription elongation to go through methylated CpG islands in the gene bodies. One typical example is that H2A.B regulates transcription elongation at imprinted loci. We found H2A.B enriched in some methylated loci. Using ChIP-seq and MeDIP-seq, we test the correlation of H2A.B and DNA methylation.
2013-12-24 | E-GEOD-48892 | biostudies-arrayexpress
Project description:H2A.B is a unique histone H2A variant that shares only 40 ~ 50 % sequence identity with canonical H2A. It has only been identified in mammals and has quickly evolved with remarkable sequence diversity among different species. H2A.B is ubiquitously expressed in most cells and tissues. It is mainly deposited in gene body region. The localization of H2A.B is associated with methylated CpG islands in mouse ES cells. H2A.B facilitates transcription elongation to go through methylated CpG islands in the gene bodies. One typical example is that H2A.B regulates transcription elongation at imprinted loci.
2013-12-24 | GSE48892 | GEO
Project description:H2ABbd is a unique histone H2A variant that shares only 40 ~ 50 % sequence identity with canonical H2A. It has only been identified in mammals and has quickly evolved with remarkable sequence diversity among different species. H2ABbd is ubiquitously expressed in most cells and tissues. It is mainly deposited in gene body region.The localization of H2ABbd is associated with methylated CpG islands in mouse ES cells.H2ABbd facilitates transcription elongation to go through methylated CpG islands in the gene bodies. One typical example is that H2ABbd regulates transcription elongation at imprinted loci.
2016-03-06 | GSE45574 | GEO
Project description:H2A.B is a unique histone H2A variant that shares only 40 ~ 50 % sequence identity with canonical H2A. It has only been identified in mammals and has quickly evolved with remarkable sequence diversity among different species. H2A.B is ubiquitously expressed in most cells and tissues. It is mainly deposited in gene body region.The localization of H2A.B is associated with methylated CpG islands in mouse ES cells.H2A.B facilitates transcription elongation to go through methylated CpG islands in the gene bodies. One typical example is that H2A.B regulates transcription elongation at imprinted loci. We used microarray to test the function of H2A.B on gene expression. Mouse ES cells infected with control knockdown(KD) or H2A.B KD virus were treated with G418. ES cells were extracted for RNA and hybridization on Affymetrix microarrays.
2013-12-24 | E-GEOD-48446 | biostudies-arrayexpress
Project description:H2A.B is a unique histone H2A variant that shares only 40 ~ 50 % sequence identity with canonical H2A. It has only been identified in mammals and has quickly evolved with remarkable sequence diversity among different species. H2A.B is ubiquitously expressed in most cells and tissues. It is mainly deposited in gene body region.The localization of H2A.B is associated with methylated CpG islands in mouse ES cells.H2A.B facilitates transcription elongation to go through methylated CpG islands in the gene bodies. One typical example is that H2A.B regulates transcription elongation at imprinted loci. We used microarray to test the function of H2A.B on gene expression.
2013-12-24 | GSE48446 | GEO
Project description:Transcription factors guide tissue development by binding to developmental stage-specific targets and establishing an appropriate enhancer landscape. In turn, DNA and chromatin modifications direct the genomic binding of transcription factors. However, how transcription factors navigate chromatin features to selectively bind a small subset of all the possible genomic target loci remains poorly understood. Here we show that Cdx2 - a lineage defining transcription factor that binds distinct targets in developing versus adult intestinal epithelial cells - has a preferential affinity for a non-canonical CpG-containing motif in vivo. A higher frequency of this motif at embryonic Cdx2 targets and methylated state of the CpG during development enables selective Cdx2 binding and activation of developmental enhancers and genes. In adult cells, demethylation at these enhancers prevents ectopic Cdx2 binding, instead directing Cdx2 to its canonical motif without a CpG. This shift in Cdx2 binding facilitates Ctcf and Hnf4 recruitment, establishing super-enhancers during development and homeostatic enhancers in adult cells, respectively. Induced DNA methylation in adult mouse epithelium or cultured cells recruits Cdx2 to developmental targets, promoting corecruitment of partner transcription factors. Thus, Cdx2’s differential CpG motif preferences enable it to navigate distinct DNA methylation profiles, activating genes specific to appropriate developmental stages.
2024-11-28 | GSE253736 | GEO
Project description:Mutations in MECP2 cause the autism-spectrum disorder Rett syndrome. MeCP2 is predicted to bind to methylated promoters and silence transcription. However, the first large-scale mapping of neuronal MeCP2-binding sites on 26.3 Mb of imprinted and nonimprinted loci revealed that 59% of MeCP2-binding sites are outside of genes and that only 6% are in CpG islands. Integrated genome-wide promoter analysis of MeCP2 binding, CpG methylation, and gene expression revealed that 63% of MeCP2-bound promoters are actively expressed and that only 6% are highly methylated. These results indicate that the primary function of MeCP2 is not the silencing of methylated promoters. Keywords: ChIP-chip analysis
2007-12-05 | GSE9568 | GEO
Project description:The enhancer/promoter of the vitellogenin II (VTG) gene has been extensively studied as a model system of vertebrate transcriptional control. While deletion mutagenesis and in vivo footprinting identified the transcription factor (TF) binding sites governing its tissue specificity, DNase hypersensitivity- and DNA methylation studies revealed the epigenetic changes accompanying its hormone-dependent activation. Moreover, upon induction with estrogen (E2), the region flanking the estrogen-responsive element (ERE) was reported to undergo active DNA demethylation. We now show that although the VTG ERE is methylated in embryonic chicken liver and in LMH/2A hepatocytes, its induction by E2 was not accompanied by extensive demethylation. In contrast, E2 failed to activate a VTG enhancer/promoter-controlled luciferase reporter gene methylated by SssI. Surprisingly, this inducibility difference could be traced not to the ERE, but rather to a single CpG in an E-box (CACGTG) sequence upstream of the VTG TATA box, which is unmethylated in vivo, but methylated by SssI. We demonstrate that this E-box binds the upstream stimulating factor USF1/2. Selective methylation of the CpG within this binding site with an E-box-specific DNA methyltranferase Eco72IM was sufficient to attenuate USF1/2 binding in vitro and abolish the hormone-induced transcription of the VTG gene in the reporter system.
2020-05-27 | PXD015594 | Pride
Project description:Genomic imprinting is controlled by CpG-rich regions (ICRs) acquiring differential methylation in the female and male germline and maintaining it in a parental origin-specific manner in somatic cells. Despite their expected mutation rate due to spontaneous deamination of methylated cytosines, ICRs maintain their CpG-richness and show conservation of CpG-bearing transcription binding sites in mammals. In order to gain further insights into the mechanisms of maintenance of methyl CpGs, we sought to identify the proteins interacting with the methylated allele of the ICRs, by determining the interactors of ZFP57 that recognizes a specific methylated ICR motif in mouse ESCs. Several proteins including factors involved in mRNA processing/splicing, chromatin organization, transcription and DNA repair were identified through a tagged approach coupled to LC–MS/MS analysis. The demonstration of the components of the post-replicative mismatch-repair (MMR) complex as ZFP57 interactors prompted us to investigate the DNA binding profile of MSH2 and MSH6 by chromatin immunoprecipitation and sequencing. We found that these proteins were enriched at the methylated allele of the ICRs and their binding was mediated by the ZFP57/KAP1 complex, suggesting that the MMR complex is recruited to these loci to preserve their genetic integrity.
2022-08-16 | GSE205041 | GEO
Project description:Astrocytomas are common and lethal human brain tumors. Here, we have analyzed the methylation status of over 28,000 CpG islands and 18,000 promoters in normal human brain and in astrocytomas of various grades using the methylated-CpG island recovery assay (MIRA). We identified six to seven thousand methylated CpG islands in normal human brain. ~5% of the promoter-associated CpG islands in normal brain are methylated. Promoter CpG island methylation is inversely and intragenic methylation is directly correlated with gene expression levels in brain tissue. In astrocytomas, several hundred CpG islands undergo specific hypermethylation relative to normal brain with 428 methylation peaks common to more than 25% of the tumors. Genes involved in brain development and neuronal differentiation, such as POU4F3, GDNF, OTX2, NEFM, CNTN4, OTP, SIM1, FYN, EN1, CHAT, GSX2, NKX6-1, RAX, PAX6, DLX2, were strongly enriched among genes frequently methylated in tumors. There was an overrepresentation of homeobox genes and 31% of the most commonly methylated genes represent targets of the Polycomb complex. We identified several chromosomal loci in which many (sometimes more than 20) consecutive CpG islands were hypermethylated in tumors. Seven of such loci were near homeobox genes, including the HOXC and HOXD clusters, and the BARHL2, DLX1, and PITX2 genes. Two other clusters of hypermethylated islands were at sequences of recent gene duplication events. Our analysis offers mechanistic insights into brain neoplasia suggesting that methylation of genes involved in neuronal differentiation, perhaps in cooperation with other oncogenic events, may shift the balance from regulated differentiation towards gliomagenesis. Comparison of methylation patterns of 30 astrocytomas and 6 controls
2010-05-16 | E-GEOD-19391 | biostudies-arrayexpress