Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA383124 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5453590.fastq.gz | Fastqsanger.gz | |||
| SRR5453600.fastq.gz | Fastqsanger.gz | |||
| SRR5453610.fastq.gz | Fastqsanger.gz | |||
| SRR5453591.fastq.gz | Fastqsanger.gz | |||
| SRR5453601.fastq.gz | Fastqsanger.gz |
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Project description:Replication-independent histone turnover confers regulatory genome for adult heart homeostasis
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Project description:Replication-independent histone turnover confers regulatory genome for adult heart homeostasis [ChIP-Seq]
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Project description:Through integrated H2BGFP ChIP-seq data over multiple conditions and time points, as well as other related ChIP-seq and RNA-seq data in adult mouse heart. We observed genomewide and locus-specific H2B turnover in non-proliferating adult cardiomyocytes (Cms), and a majority of genomic regions with rapid turnover rates distributes on cis-regulatory elements, as well as these regions are associated with heart function, regulatory factors binding and their activities. Moreover, H2B turnover rate is always positively correlated with gene transcription level on enhancers, promoters and exons. The rapid turnover rates at cis-regulatory elements can be partially explained by the binding and co-binding of RNAP II and various transcription factors (TFs). Our further analysis revealed that not only rapid H2B turnover at cis-regulatory elements responses to heart disease, but also slow turnover at H3K27me3 sites functionally responses to heart disease with a different manner. More generally, we indicate that the binding and co-binding of DNA-binding proteins, such as TFs and epigenetic enzymes, all of them coupled with H2B turnover to modulate gene transcription and chromatin state.
2020-04-17 | GSE97876 | GEO
Project description:Disruption and replacement of nucleosomal histone (histone turnover, HT) take place during transcription and cell division. Here we examined the functional roles for replication-independent HT in directing precise regulatory genome in terminally differentiated cardiomyocytes (CMs) of adult heart. Surprisingly, histone H2B pausing and chasing assay revealed the histone halftime ~2.5 weeks in non-replicating CMs, in sharp contrast to the longer halftime of CMs, despite in the abscence of replication-dependent passive dilution of labeled histones. Regions of high HT identified enhancers of important heart function. Co-occupancy of mutiple cardiac transcription factors in part accounted for enhancers on sites lacking nucleosome eviction by passage of RNA polymerase II. Unexpectedly, both polycomb EED and HDACs augmented HT rate in bufferring poised enhancer activition without alteration of nucleosome occupancy. Thus, our results suggest replication-indenpendent HT as an additional layer of chromatin-based regulation of functional homeostasis.
2019-06-14 | GSE103680 | GEO
Project description:Disruption and replacement of nucleosomal histone (histone turnover, HT) take place during transcription and cell division. Here we examined the functional roles for replication-independent HT in directing precise regulatory genome in terminally differentiated cardiomyocytes (CMs) of adult heart. Surprisingly, histone H2B pausing and chasing assay revealed the histone halftime ~2.5 weeks in non-replicating CMs, in sharp contrast to the longer halftime of CMs, despite in the abscence of replication-dependent passive dilution of labeled histones. Regions of high HT identified enhancers of important heart function. Co-occupancy of mutiple cardiac transcription factors in part accounted for enhancers on sites lacking nucleosome eviction by passage of RNA polymerase II. Unexpectedly, both polycomb EED and HDACs augmented HT rate in bufferring poised enhancer activition without alteration of nucleosome occupancy. Thus, our results suggest replication-indenpendent HT as an additional layer of chromatin-based regulation of functional homeostasis.
2019-06-14 | GSE103679 | GEO
Project description:Nucleosome turnover concomitant with incorporation of the replication-independent histone variant H3.3 is a hallmark of regulatory regions in the animal genome. In our current understanding, nucleosome turnover is universally linked to DNA accessibility and histone acetylation. In mouse embryonic stem cells, H3.3 is also highly enriched at interstitial heterochromatin, most prominently intracisternal-A particle endogenous retroviral elements. Interstitial heterochromatin is established over confined domains by the TRIM28/SETDB1 corepressor complex and has stereotypical features of repressive chromatin, such as H3K9me3 and recruitment of all HP1 isoforms. Here, we demonstrate that fast histone turnover and H3.3 incorporation is compatible with these hallmarks of heterochromatin. We identify Smarcad1 to be a chromatin remodeler that generates nucleosome-free regions which are subsequently filled with histone H3.3, generating a surprisingly dynamic heterochromatin state. Loss of histone H3.3 elicits a highly specific opening of interstitial heterochromatin demonstrating that in the wake of Smarcad1 remodeling, H3.3 is required to maintain minimal DNA accessibility by reassembling nucleosomes.
2020-08-28 | GSE149080 | GEO
Project description:We developed a system to study the DNA replication-independent turnover nucleosomes containing the histone variant H3.3 in mammalian cells. By measuring the genome-wide incorporation of H3.3 at different time points following epitope-tagged H3.3 expression, we find three categories of H3.3-nucleosome turnover in vivo: rapid turnover, intermediate turnover and, specifically at telomeres, slow turnover. Our data indicate that H3.3-containing nucleosomes at enhancers and promoters undergo a rapid turnover that is associated with active histone modification marks including H3K4me1, H3K4me3, H3K9ac, H3K27ac and the histone variant H2A.Z. The rate of turnover is negatively correlated with H3K27me3 at regulatory regions and with H3K36me3 at gene bodies.
2013-10-23 | GSE51505 | GEO
Project description:We developed a system to study the DNA replication-independent turnover nucleosomes containing the histone variant H3.3 in mammalian cells. By measuring the genome-wide incorporation of H3.3 at different time points following epitope-tagged H3.3 expression, we find three categories of H3.3-nucleosome turnover in vivo: rapid turnover, intermediate turnover and, specifically at telomeres, slow turnover. Our data indicate that H3.3-containing nucleosomes at enhancers and promoters undergo a rapid turnover that is associated with active histone modification marks including H3K4me1, H3K4me3, H3K9ac, H3K27ac and the histone variant H2A.Z. The rate of turnover is negatively correlated with H3K27me3 at regulatory regions and with H3K36me3 at gene bodies. Examination of incorporation dynamics of histone variant H3.3
2013-10-23 | E-GEOD-51505 | biostudies-arrayexpress
Project description:Acetylation of histone H3 lysine 56 is a covalent modification best-known as a mark of newly-replicated chromatin, but has also been linked to replication-independent histone replacement. Here, we measured H3K56ac levels at single-nucleosome resolution in asynchronously growing yeast cultures, as well as in yeast proceeding synchronously through the cell cycle. We developed a quantitative model of H3K56ac kinetics, which shows that H3K56ac is largely explained by the genomic replication timing and the turnover rate of each nucleosome, suggesting that cell cycle profiles of H3K56ac should reveal most first-time nucleosome incorporation events. However, since the deacetylases Hst3/4 prevent use of H3K56ac as a marker for histone deposition during M phase, we also directly measured M phase histone replacement rates. We report a global decrease in turnover rates during M phase, and a further specific decrease in turnover among early origins of replication, which switch from rapidly-replaced in G1 phase to stable-bound during M phase. Finally, by measuring H3 replacement in yeast deleted for the H3K56 acetyltransferase Rtt109 and its two co-chaperones Asf1 and Vps75, we find evidence that Rtt109 and Asf1 preferentially enhance histone replacement at rapidly-replaced nucleosomes, whereas Vps75 appears to inhibit histone turnover at those loci. These results provide a broad perspective on histone replacement/incorporation throughout the cell cycle, and suggest that H3K56 acetylation provides a positive feedback loop by which replacement of a nucleosome enhances subsequent replacement at the same location.
2008-10-04 | GSE12822 | GEO