Ontology highlight
ABSTRACT:
PROVIDER: PRJNA934392 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23447714_1.fastq.gz | Fastqsanger.gz | |||
| SRR23447714_2.fastq.gz | Fastqsanger.gz | |||
| SRR23447715_1.fastq.gz | Fastqsanger.gz | |||
| SRR23447715_2.fastq.gz | Fastqsanger.gz | |||
| SRR23447716_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:H3K27ac modified nucleosomes are a major epigenetic mark of active chromatin that can be used to identify cell type specific chromatin regulatory regions which serve as binding sites for transcription factors. Here we show that H3K27ac modified nucleosomes recruit the ubiquitous nucleosome binding proteins HMGN1 and HMGN2 to cell-type specific chromatin regulatory regions. We find that HMGNs bind directly to the acetylated nucleosome and that the H3K27ac residue and linker DNA are necessary and sufficient for the preferential binding of HMGNs to the modified nucleosomes. Loss of HMGNs increases the levels of H3K27me3 and the histone H1 occupancy at enhancers and promoters and alters the interaction of several transcription factors with chromatin. These experiments identify an additional mechanism whereby the H3K27ac epigenetic mark promotes chromatin decompaction and provide insights into the molecular mechanism whereby HMGN proteins, which bind to chromatin without DNA sequence specificity, modulate cell type specific gene expression.
2020-09-20 | GSE156697 | GEO
Project description:DNA methylation and histone modification exert epigenetic control over gene expression. CHG methylation by CHROMOMETHYLASE3 (CMT3) depends on histone H3K9 dimethylation (H3K9me2), but the mechanism underlying this relationship is poorly understood. Here, we report multiple lines of evidence that CMT3 interacts with H3K9me2-containing nucleosomes. CMT3 genome locations nearly perfectly correlated with H3K9me2 and CMT3 stably associated with H3K9me2-containing nucleosomes. Crystal structures of maize CMT3 homologue, ZMET2, in complex with H3K9me2 peptides, showed that ZMET2 binds H3K9me2 via both BAH and chromo domains. The structures reveal an aromatic cage within both BAH and chromo domains as interaction interfaces that capture H3K9me2. Mutations that abolish either interaction disrupt CMT3 binding to nucleosomes, and show a complete loss of CMT3 activity in vivo. Our study establishes dual recognition of H3K9me2 marks by BAH and chromo domains, and reveals a novel mechanism of interplay between DNA methylation and histone modification. Investigation of genome-wide occupancy of CMT3 by ChIP-seq
2012-11-11 | E-GEOD-39097 | biostudies-arrayexpress
Project description:DNA methylation and histone modification exert epigenetic control over gene expression. CHG methylation by CHROMOMETHYLASE3 (CMT3) depends on histone H3K9 dimethylation (H3K9me2), but the mechanism underlying this relationship is poorly understood. Here, we report multiple lines of evidence that CMT3 interacts with H3K9me2-containing nucleosomes. CMT3 genome locations nearly perfectly correlated with H3K9me2 and CMT3 stably associated with H3K9me2-containing nucleosomes. Crystal structures of maize CMT3 homologue, ZMET2, in complex with H3K9me2 peptides, showed that ZMET2 binds H3K9me2 via both BAH and chromo domains. The structures reveal an aromatic cage within both BAH and chromo domains as interaction interfaces that capture H3K9me2. Mutations that abolish either interaction disrupt CMT3 binding to nucleosomes, and show a complete loss of CMT3 activity in vivo. Our study establishes dual recognition of H3K9me2 marks by BAH and chromo domains, and reveals a novel mechanism of interplay between DNA methylation and histone modification.
2012-11-11 | GSE39097 | GEO
Project description:ChIP-Sequencing using antibody to H3K9ac,H3K27ac,H3K4me3, H3K79me2, H3K9me2, H3K9me3 and H3K27me3 in cardiomyocytes isolated from mice after 1 week of transverse aortic constriction (TAC) and in control mice (sham).
2013-11-30 | E-MTAB-1506 | biostudies-arrayexpress
Project description:Our understanding of the functions of DNA elements is limited by the paucity of information about the spectrum of proteins that occupy these genomic regions. Here we describe an approach to identify proteins associated with genomic regions whose chromatin is marked by specific modified histones, which we term chromatin profiling. We used chromatin immunoprecipitation followed by mass spectrometry (ChIP-MS) to identify proteins associated with genomic regions marked by histone H3K27Ac, H3K4me3, H3K79me2 and H3K36me3 in mouse embryonic stem (mES) cells. We identified 385 known and 224 novel candidate proteins associated with these histone-marked genomic segments and confirmed that several of the novel candidates are indeed associated with histone-marked segments of the genome. Future study of the novel candidates, many of which have been implicated in various diseases, should lead to an improved understanding of gene control and its dysregulation in disease. ChIP-seq for nucleosomes with modified histones and DNA-binding proteins in mouse embryonic stem cells, and DNA-binding proteins in Jurkat cells
2015-02-05 | E-GEOD-62380 | biostudies-arrayexpress
Project description:Recruitment of HMGN By H3K27ac Modified Nucleosomes to Regulatory Sites Modulates Transcription Factor Binding to Chromatin
| PRJNA658791 | ENA
Project description:Histone post-translational modifications (PTM) encode much of genome's regulatory information. However, regular chromatin immunoprecipitation followed by sequencing (ChIP-seq) protocols trace histone PTM to genomic regions spanning several nucleosomes, making it difficult to study how different histone PTM combine within individual nucleosomes to regulate the genome. Here, we devised computational and statistical methods to map H3K4me3, H3K27Ac, H3K9me3, and H3K27me3 to individual nucleosomes using MNase digestion of chromatin coupled with ChIP-seq. A significant number of nucleosomes were marked by two or more of histone marks. Nucleosomes marked simultaneously by H3K4me3 and H3K27me3 were prevalent among bivalent domains compared to the genomic background whereas nucleosomes having the repressive marks H3K27me3 and H3K9me3 were enriched at the transcription staring site of highly active genes only if they were also co-localized with the activating mark H3K27Ac. Inclusion of alternatively spliced exons on the final mRNA is correlated with nucleosomes marked by H3K4me3, H3K27Ac, and H3K27me3, but is largely unaffected by nucleosomes marked by H3K9me3. Together, these findings reveal that combinatorial patterns of histone PTM within individual nucleosomes are fundamental to encode regulatory information.
2018-09-14 | GSE73004 | GEO
Project description:Established dogma holds that all facets of chromatin organization and histone posttranslational modification are complete before sperm exits the testes. Using proteomic analysis to contrast immature spermatozoa and mature sperm from the epididymis, we find progressive changes in multiple histone posttranslational modifications, including H3K4me1, H3K27ac H3K79me2, H3K64ac, H3K122ac, H4K16ac, H3K9me2, and H4K20me3. In contrast, levels of H3K4me3 and H3K27me3 remained constant. Using chromatin immunoprecipitation coupled with deep sequencing, we find that changes in H3K27ac and H3K9me2 involve sharpening broad diffuse regions into narrow peaks, centered on promoters and distal enhancers driving embryonic development (H3K27ac) or tissue-specific genes sequestered in lamina-associated domains (H3K9me2). Maturing sperm contain the histone deacetylase enzymes HDAC1 and HDAC3, suggesting the NuRD complex may drive these changes. These data extend our understanding of germline programming and reveal that, in addition to trafficking noncoding RNAs, alterations to histone structure are a core feature of epididymal maturation.
2022-01-01 | GSE185603 | GEO
Project description:We report the distribution of histone H3K4me1 and H3K27ac within the genome of mouse embryonic midbrain. We prepared the chromatin from 11 dpc embryonic midbrain and made chromatin precipitation with antibody against H3K4me1 and H3K27ac (rabbit polyclonal antibody). High-throughput sequencing applied for the ChIP analysis revealed the differential distribution of modified histone within developing midbrain. ChIP analysis of mouse 11 dpc embryonic midbrain and forelimb buds against anti-H3K4me1 and H3K27ac antibody.
2014-01-15 | E-GEOD-49652 | biostudies-arrayexpress
Project description:We identified KDM3A, a demethylase of histone H3K9me1/2, as a positive regulator for hippo target genes. We found that H3K27ac upregulation is highly correlated with gene activation, but not H3K4me3; and transcription repression of certain TEAD1 target genes, such as BBC3, is important for the pathway function. KDM3A knockout caused upregulation of H3K9me2 mainly on TEAD1-binding enhancers rather than gene bodies, leading to decrease of H3K27ac and TEAD1 binding on enhancers and impaired transcription. We identified KDM3A, a demethylase of histone H3K9me1/2, as a positive regulator for hippo target genes. We found that H3K27ac upregulation is highly correlated with gene activation, but not H3K4me3; and transcription repression of certain TEAD1 target genes, such as BBC3, is important for the pathway function. KDM3A knockout caused upregulation of H3K9me2 mainly on TEAD1-binding enhancers rather than gene bodies, leading to decrease of H3K27ac and TEAD1 binding on enhancers and impaired transcription.
2019-03-20 | GSE108920 | GEO