Histone variant H3.3 facilitates open chromatin at promoters [CUT&TAG]
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE213039 | GEO | 2023/01/25
REPOSITORIES: GEO
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Project description:We analyze the contribution of H3.3 to chromatin accessibility, post-translational modification states, and transcription in mouse embryonic stem cells (mESC).
2023-01-25 | GSE186686 | GEO
Project description:We analyze the contribution of H3.3 to chromatin accessibility, post-translational modification states, and transcription in mouse embryonic stem cells (mESC).
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Project description:We analyze the contribution of H3.3 to chromatin accessibility, post-translational modification states, and transcription in mouse embryonic stem cells (mESC).
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Project description:This SuperSeries is composed of the SubSeries listed below.
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Project description:Zygotic gene activation (ZGA) is the first transcription event in life, and is associated with extensive epigenetic reprogramming, which is involved with dynamic incorporation of histone variant H3.3. H3.3 plays essential roles during mouse pre-implantation development. However, the coexistence of distinct sources of H3.3 in early embryos, including paternal and maternal allele-expressed H3.3 (paH3.3 and maH3.3), complicates our ability to track their individual dynamics, which may have distinct roles in embryonic development. In this study, by taking advantage of our H3.3B-HA-tagged mouse model, we illustrated the paH3.3 and maH3.3 landscapes in mouse early embryos, and described the manner of maternal mRNAs-derived H3.3 (mH3.3) on paternal genome reprogramming. We found the deposition of mH3.3 is required for cleavage development and minor ZGA, mechanistically, by mH3.3S31p-meditated acetylation at lysine 27. And, we propose that the mH3.3K27ac modification displaces the repressive histone modifications, thus enabling the activation of minor ZGA genes. Taken together, we demonstrate the central role of mH3.3 in reprogramming parental genomes by establishment of H3K27ac.
2024-09-12 | GSE242958 | GEO
Project description:The incorporation of histone H3 variants has been implicated in the epigenetic memory of cellular state. Using genome editing with zinc finger nucleases to tag endogenous H3.3, we report genome-wide profiles of H3 variants in mammalian embryonic stem (ES) cells and neuronal precursor cells. Genome-wide patterns of H3.3 are dependent on amino acid sequence, and change with cellular differentiation at developmentally regulated loci. The H3.3 chaperone Hira is required for H3.3 enrichment at active and repressed genes. Strikingly, Hira is not essential for localization of H3.3 at telomeres and many transcription factor binding sites. Immunoaffinity purification and mass spectrometry reveal that the proteins Atrx and Daxx associate with H3.3 in a Hira-independent manner. Atrx is required for Hira-independent localization of H3.3 at telomeres, and for the repression of telomeric RNA. Our data demonstrate that multiple and distinct factors are responsible for H3.3 localization at specific genomic locations in mammalian cells. Crosslinking ChIP-seq: Examination of 1 histone variant (H3.3), 2 histone modifications, and Serine-5 phosphorylated RNA polymerase in 2 different cell types (H3.3-HA ES samples 1-4, and H3.3-HA NPC samples 7-10). Examination of 1 histone variant (H3.2), and one histone modification (H3K36me3) in 2 different cell types (H3.2-HA ES samples 5-6, and H3.2-HA NPC samples 11-12). Examination of 1 histone variant (H3.3), input control, and one histone modification (H3K36me3) in one cell type (H3.3-HA hybrid ES, samples 13-15). Examination of 1 histone variant (H3.1S31), input control, and one histone modification (H3K36me3) in one cell type (H3.1S31-HA hybrid ES, samples 16-18). Native ChIP-seq: Examination of 1 histone variant (H3.3), input control, and one histone modification (H3K4me3) in one cell type (H3.3-HA ES, samples 19-21). Examination of 1 histone variant (H3.2), input control, and two histone modifications (H3K4me3 and H3K27me3) in one cell type (H3.2-HA ES, samples 22-25). Examination of 1 histone variant (H3.3), input control, and two histone modifications (H3K4me1 and H3K36me3) in one cell type (H3.3-EYFP ES, samples 26-29). Examination of 1 histone variant (H3.3), input control, and two histone modifications (H3K4me1 and H3K36me3) in one cell type (Hira -/- H3.3-EYFP ES, samples 30-33). Examination of 1 histone variant (H3.3) and input control in one cell type (Atrxflox H3.3-EYFP ES, samples 34-37). Examination of HA antibody background in one cell type (wild-type ES, sample 38).
2010-03-04 | E-GEOD-16893 | biostudies-arrayexpress
Project description:Mature oocyte cytoplasm can reprogram somatic cell nuclei to the pluripotent state through a series of sequential events including protein exchange between the donor nucleus and ooplasm, chromatin remodeling, and pluripotency gene reactivation. Maternal factors that are responsible for this reprogramming process remain largely unidentified. Here, we demonstrate that knockdown of histone variant H3.3 in mouse oocytes results in compromised reprogramming and down-regulation of key pluripotency genes; and this compromised reprogramming both for developmental potentials and transcription of pluripotency genes can be rescued by injecting exogenous H3.3 mRNA, but not H3.2 mRNA into oocytes in somatic cell nuclear transfer (SCNT) embryos. We show that maternal H3.3, and not H3.3 in the donor nucleus, is essential for successful reprogramming of somatic cell nucleus into the pluripotent state. Furthermore, H3.3 is involved in this reprogramming process by remodeling the donor nuclear chromatin through replacement of donor nucleus-derived H3 with de novo synthesized maternal H3.3 protein. Our study shows that H3.3 is a crucial maternal factor for oocyte reprogramming and provides a practical model to directly dissect the oocyte for its reprogramming capacity. Transcriptome sequencing of 4-cell NT embryos, Luciferase 4-cell SCNT embryos, 4-cell NT embryos_H3.3KD, 4-cell NT embryos_H3.3KD+H3.3mRNA, H3.3 KD + H3.2 mRNA SCNT embryos
2014-06-02 | E-GEOD-56762 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE16882: Histone H1 binding is restricted by histone variant H3.3 (Nucleosome) GSE16883: Histone H1 binding is restricted by histone variant H3.3 (DamID) GSE16884: Histone H1 binding is restricted by histone variant H3.3 (Expression) GSE19764: Histone H1 binding is restricted by histone variant H3.3 (FAIRE) Refer to individual Series
2009-10-15 | E-GEOD-16885 | biostudies-arrayexpress
Project description:In animals, replication coupled histone H3.1 can be distinguished from replication independent histone H3.3. H3.3 variants are enriched at active genes and their promoters. Furthermore, H3.3 is specifically incorporated upon gene activation. Histone H3 variants evolved independently in plants and animals and it is unclear whether different replication independent H3.3 variants developed similar properties in both phyla. We studied Arabidopsis H3 variants in order to find core properties of this class of histones. Here we present genome-wide maps of H3.3 and H3.1 enrichment and the dynamic changes of their profiles upon cell division arrest. We find H3.3 enrichment to positively correlate with gene expression and to be biased towards the transcription termination site. While heterochromatic regions are mostly depleted of H3.3, H3.1 shows a more even distribution along the genome. We report that in planta, dynamic changes in H3.3 profiles are associated with the extensive remodeling of the transcriptome that occurs during cell differentiation. We propose that H3.3 dynamics are linked to transcription and are involved in resetting covalent histone marks at a genomic scale during plant development. Similarities between plant and animal H3.3 deposition profiles indicate that H3 variants likely result from functionally convergent evolution. Analysis of 2 different histone H3 variants and transcriptome in 2 conditions.
2012-05-15 | E-GEOD-36626 | biostudies-arrayexpress
Project description:In animals, replication coupled histone H3.1 can be distinguished from replication independent histone H3.3. H3.3 variants are enriched at active genes and their promoters. Furthermore, H3.3 is specifically incorporated upon gene activation. Histone H3 variants evolved independently in plants and animals and it is unclear whether different replication independent H3.3 variants developed similar properties in both phyla. We studied Arabidopsis H3 variants in order to find core properties of this class of histones. Here we present genome-wide maps of H3.3 and H3.1 enrichment and the dynamic changes of their profiles upon cell division arrest. We find H3.3 enrichment to positively correlate with gene expression and to be biased towards the transcription termination site. While heterochromatic regions are mostly depleted of H3.3, H3.1 shows a more even distribution along the genome. We report that in planta, dynamic changes in H3.3 profiles are associated with the extensive remodeling of the transcriptome that occurs during cell differentiation. We propose that H3.3 dynamics are linked to transcription and are involved in resetting covalent histone marks at a genomic scale during plant development. Similarities between plant and animal H3.3 deposition profiles indicate that H3 variants likely result from functionally convergent evolution. Analysis of 2 different histone H3 variants and transcriptome in 2 conditions.
2012-05-15 | E-GEOD-36629 | biostudies-arrayexpress