Mus musculus
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR013107.fastq.gz | Fastqsanger.gz | |||
| DRR013108.fastq.gz | Fastqsanger.gz | |||
| DRR013109.fastq.gz | Fastqsanger.gz | |||
| DRR013110.fastq.gz | Fastqsanger.gz | |||
| DRR013111.fastq.gz | Fastqsanger.gz |
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Project description:Replication-independent deposition of histone variant H3.3 into chromatin is essential for many biological processes, including development, oogenesis and nuclear reprogramming. Unlike replication-dependent H3.1/2 isoforms, H3.3 is expressed throughout the cell cycle and becomes enriched in postmitotic cells with age. However, lifelong dynamics of H3 variant replacement and the impact of this process on chromatin organization remain largely undefined. To address this, we investigated genome-wide changes in histone H3 variants composition and H3 modification abundances throughout the lifespan in mice using quantitative mass spectrometry (MS) – based middle-down proteomics strategy. Using middle-down MS we demonstrate that H3.3 accumulates in the chromatin of various somatic mouse tissues throughout life, resulting in near complete replacement of H3.1/2 isoforms by the late adulthood. Accumulation of H3.3 is associated with profound changes in the global level of H3 methylation. H3.3-containing chromatin exhibits distinct stable levels of H3R17me2 and H3K36me2, different from those on H3.1/H3.2-containing chromatin, indicating a direct link between H3 variant exchange and histone methylation dynamics with age. In summary, our study provides the first time comprehensive characterization of dynamic changes in the H3 modification landscape during mouse lifespan and links these changes to the age-dependent accumulation of histone variant H3.3.
2017-07-28 | PXD005300 | Pride
Project description:The histone variant H2A.Z plays key roles in gene expression, DNA repair, and centromere function. H2A.Z deposition is controlled by SWR-C chromatin remodeling enzymes that catalyze the nucleosomal exchange of canonical H2A with H2A.Z. Here we report that acetylation of histone H3 lysine 56 (H3-K56Ac) alters the substrate specificity of SWR-C, leading to promiscuous dimer exchange where either H2A.Z or H2A can be exchanged from nucleosomes. This result is confirmed in vivo, where genome-wide analysis demonstrates widespread decreases in H2A.Z levels in yeast mutants with hyperacetylated H3K56. Our work also suggests that a conserved SWR-C subunit may function as a M-bM-^@M-^\lockM-bM-^@M-^] that prevents removal of H2A.Z from nucleosomes. Our study identifies a histone modification that regulates a chromatin remodeling reaction and provides insights into how histone variants and nucleosome turnover can be controlled by chromatin regulators. H2A.Z ChIP seq experiments in mutants with constitutive H3K56ac
2013-04-15 | E-GEOD-43935 | biostudies-arrayexpress
Project description:How histone intrinsic sequence variation or regulatory modifications regulate nucleosome interactions with transcription remain unclear. To clarify this question, we examined how histone variants and histone modifications assemble in the Arabidopsis thaliana genome, identifying a limited number of chromatin states that divide euchromatin and heterochromatin in biologically significant subdomains. We showed that histone variants were as significant as histone modifications to determine the composition of chromatin states. The loss of function of the chromatin remodeler DECREASED IN DNA METHYLATION (DDM1) prevented the exchange between the histone variants H2A.Z and H2A.W over transposons resulting in their enrichment in chromatin states found only on proteins coding genes in the wild type. Hence, the dynamics of histone H2A variants exchange impacted the definition and distribution of chromatin states. We propose that dynamics of histone variants control the organization of histone modifications into chromatin states to achieve landmarks that signify the ability for transcription. Chromatin immunoprecipitation sequencing (ChIP-seq) for histone H2A variants and histone modifications in Col0 and ddm1(-/-) .
2023-05-09 | GSE231398 | GEO
Project description:How histone intrinsic sequence variation or regulatory modifications regulate nucleosome interactions with transcription remain unclear. To clarify this question, we examined how histone variants and histone modifications assemble in the Arabidopsis thaliana genome, identifying a limited number of chromatin states that divide euchromatin and heterochromatin in biologically significant subdomains. We showed that histone variants were as significant as histone modifications to determine the composition of chromatin states. The loss of function of the chromatin remodeler DECREASED IN DNA METHYLATION (DDM1) prevented the exchange between the histone variants H2A.Z and H2A.W over transposons resulting in their enrichment in chromatin states found only on proteins coding genes in the wild type. Hence, the dynamics of histone H2A variants exchange impacted the definition and distribution of chromatin states. We propose that dynamics of histone variants control the organization of histone modifications into chromatin states to achieve landmarks that signify the ability for transcription. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for histone H2A variants and histone modifications in seedlings .
2023-05-09 | GSE226469 | GEO
Project description:Endogenous retroviruses (ERVs) were usually silenced by various histone modifications on histone H3 variants and respective histone chaperones in embryonic stem cells (ESCs). However, it is still unknown whether chaperones of other histones could repress ERVs. Here, we show that H2A/H2B histone chaperone FACT plays a critical role in silencing ERVs and ERV-derived cryptic promoters in ESCs. Loss of FACT component Ssrp1 activated MERVL whereas the re-introduction of Ssrp1 rescued the phenotype. Additionally, Ssrp1 interacted with MERVL and suppressed cryptic transcription of MERVL-fused genes. Remarkably, Ssrp1 interacted with and recruited H2B deubiquitinase Usp7 to Ssrp1 target genes. Suppression of Usp7 caused similar phenotypes as loss of Ssrp1. Furthermore, Usp7 acted by deubiquitinating H2Bub and thereby repressed the expression of MERVL-fused genes. Taken together, our study uncovers a unique mechanism by which FACT complex silences ERVs and ERV-derived cryptic promoters in ESCs.
2020-08-24 | PXD017351 | Pride
Project description:The histone variant H2A.Z plays key roles in gene expression, DNA repair, and centromere function. H2A.Z deposition is controlled by SWR-C chromatin remodeling enzymes that catalyze the nucleosomal exchange of canonical H2A with H2A.Z. Here we report that acetylation of histone H3 lysine 56 (H3-K56Ac) alters the substrate specificity of SWR-C, leading to promiscuous dimer exchange where either H2A.Z or H2A can be exchanged from nucleosomes. This result is confirmed in vivo, where genome-wide analysis demonstrates widespread decreases in H2A.Z levels in yeast mutants with hyperacetylated H3K56. Our work also suggests that a conserved SWR-C subunit may function as a “lock” that prevents removal of H2A.Z from nucleosomes. Our study identifies a histone modification that regulates a chromatin remodeling reaction and provides insights into how histone variants and nucleosome turnover can be controlled by chromatin regulators.
2013-04-15 | GSE43935 | GEO
Project description:Nucleosomes package eukaryotic DNA and are composed of four different histone proteins, H3, H4, H2A and H2B. Histone H3 has two main variants, H3.1 and H3.3, which show different genomic localization patterns in animals. We profiled H3.1 and H3.3 variants in the genome of the plant Arabidopsis thaliana and show that the localization of these variants shows broad similarity in plants and animals, in addition to some unique features. H3.1 was enriched in silent areas of the genome including regions containing the repressive chromatin modifications H3 lysine 27 methylation, H3 lysine 9 methylation, and DNA methylation. In contrast, H3.3 was enriched in actively transcribed genes, especially peaking at the 3’ end of genes, and correlated with histone modifications associated with gene activation such as histone H3 lysine 4 methylation, and H2B ubiquitylation, as well as by RNA Pol II occupancy. Surprisingly, both H3.1 and H3.3 were enriched on defined origins of replication, as was overall nucleosome density, suggesting a novel characteristic of plant origins. Our results are broadly consistent with the hypothesis that H3.1 acts as the canonical histone that is incorporated during DNA replication, whereas H3.3 acts as the replacement histone that can be incorporated outside of S-phase during chromatin disrupting processes like transcription. ChIP-seq - 4 samples: 2 experiment and 2 controls RNA-seq - 1 sample
2012-03-05 | E-GEOD-34840 | biostudies-arrayexpress
Project description:Nuclear deubiquitinase BAP1 (BRCA1-Associated Protein 1) is a core component of multiprotein complexes that promote transcription by reversing the ubiquitination of histone 2A (H2A). BAP1 is a tumor suppressor gene whose germline loss-of-function variants predispose to cancer. To our knowledge, there are very rare examples of different germline variants in the same gene causing either a NDD or a tumor predisposition syndrome. Here, we report a series of 11 de novo germline heterozygous missense BAP1 variants associated with a rare syndromic neurodevelopmental disorder (NDD). Functional analysis showed that most of the variants cannot rescue the consequences of BAP1 inactivation, suggesting a loss-of-function mechanism. In T cells isolated from two affected children, H2A deubiquitination was impaired in matching peripheral blood mononuclear cells, histone H3 K27 acetylation ChIP-seq indicated that these BAP1 variants induced genome-wide chromatin state alterations, with enrichment for regulatory regions surrounding genes of the ubiquitin-proteasome system (UPS). Altogether, these results define a clinical syndrome caused by rare germline missense BAP1 variants that alter chromatin remodeling through abnormal histone ubiquitination and lead to transcriptional dysregulation of developmental genes.
2021-12-10 | GSE190394 | GEO
Project description:The selective incorporation of appropriate histone variants into chromatin is critical for the regulation of genome function. Although many histone variants have been identified, a complete list has not been compiled. We screened human and mouse genomes by in silico hybridization using canonical histone sequences, and found 14 uncharacterized H3-related genes in mouse. Most were similar to the H3.3 variant; their 3′ untranslated regions lacked a stem-loop structure but did have a poly- adenylation signal. Transcriptome analysis revealed tissue-specific expression of these variants. When expressed as GFP-tagged versions in mouse C2C12 cells, some variants were stably incorporated into chromatin and the genome distributions of most variants were similar to that of H3.3. Over-expression of some variants altered gene expression patterns in differentiated C2C12 cells, suggesting that these new H3 variants have specific and distinct functions.
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Project description:During DNA replication modified parental histones H3-H4 are segregated almost symmetrically to the two daughter DNA strands enabling mitotic inheritance of histone PTMs. Whether heritable histone modifications confer epigenetic regulation by maintaining chromatin states and gene expression is unclear. Using MCM2 histone-binding mutant embryonic stem cells (ESCs) and mass spectrometry, we show that asymmetric segregation of parental histones to the leading strand causes imbalanced inheritance of histone H3K27 methylations to daughter cells.
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