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Single cell RNA-Seq of Hira-KO and control MII oocytes [Gdf9-Cre+]

ABSTRACT: The integrity of chromatin, which provides a dynamic template for all DNA related processes in eukaryotes, is maintained through replication dependent and independent assembly pathways. To address the role of replication independent histone deposition, we deleted the histone H3.3 chaperone Hira in developing mouse oocytes. We show that chromatin of non-replicative developing oocytes is highly dynamic, and that lack of continuous H3.3/H4 deposition alters chromatin structure, resulting in increased DNase I sensitivity, the accumulation of DNA damage, and, ultimately, a severe fertility phenotype. On the molecular level, abnormal chromatin structure leads to a dramatic decrease in the dynamic range of gene expression, the appearance of spurious transcripts, and inefficient de novo DNA methylation. In contrast to the only minor transcriptional phenotype observed in mouse pluripotent cells, we unequivocally show the importance of histone replacement and chromatin homeostasis for transcriptional regulation and normal developmental progression in an in vivo context.

ORGANISM(S): Mus musculus

PROVIDER: GSE66931 | GEO | 2015/11/03

SECONDARY ACCESSION(S): PRJNA278394

REPOSITORIES: GEO

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Single cell RNA-Seq of Hira-KO and control MII oocytes [Gdf9-Cre+]

Project description:The integrity of chromatin, which provides a dynamic template for all DNA related processes in eukaryotes, is maintained through replication dependent and independent assembly pathways. To address the role of replication independent histone deposition, we deleted the histone H3.3 chaperone Hira in developing mouse oocytes. We show that chromatin of non-replicative developing oocytes is highly dynamic, and that lack of continuous H3.3/H4 deposition alters chromatin structure, resulting in increased DNase I sensitivity, the accumulation of DNA damage, and, ultimately, a severe fertility phenotype. On the molecular level, abnormal chromatin structure leads to a dramatic decrease in the dynamic range of gene expression, the appearance of spurious transcripts, and inefficient de novo DNA methylation. In contrast to the only minor transcriptional phenotype observed in mouse pluripotent cells, we unequivocally show the importance of histone replacement and chromatin homeostasis for transcriptional regulation and normal developmental progression in an in vivo context. RNA-Seq on 4 Hiraf/f and 4 Hiraf/f, Gdf9-Cre+ single MII oocytes

2015-11-03 | E-GEOD-66931 | biostudies-arrayexpress

Single cell RNA-Seq of Hira-KO and control MII oocytes [Zp3-Cre]

Project description:The integrity of chromatin, which provides a dynamic template for all DNA-related processes in eukaryotes, is maintained through replication-dependent and -independent assembly pathways. To address the role of replication-independent histone deposition, we deleted the histone H3.3 chaperone Hira in developing mouse oocytes. We show that chromatin of non-replicative developing oocytes is highly dynamic, and that lack of continuous H3.3/H4 deposition alters chromatin structure, resulting in increased DNase I sensitivity, the accumulation of DNA damage, and, ultimately, a severe fertility phenotype. On the molecular level, abnormal chromatin structure leads to a dramatic decrease in the dynamic range of gene expression, the appearance of spurious transcripts, and inefficient de novo DNA methylation. In contrast to the only minor transcriptional phenotype observed in mouse pluripotent cells, we unequivocally show the importance of histone replacement and chromatin homeostasis for transcriptional regulation and normal developmental progression in an in vivo context. RNA-Seq on 4 Hiraf/f and 4 Hiraf/f, Zp3-Cre single MII oocytes.

2015-11-03 | E-GEOD-73381 | biostudies-arrayexpress

Single cell RNA-Seq of Hira-KO and control MII oocytes [Zp3-Cre]

2015-11-03 | GSE73381 | GEO

Hira is essential for normal transcriptional regulation and efficient de novo DNA methylation during mouse oogenesis

2015-10-12 | GSE66629 | GEO

Histone chaperone ASF1 mediates H3.3-H4 deposition in Arabidopsis

Project description:Histone chaperones and chromatin remodelers control nucleosome dynamics, essential for transcription, replication, and DNA repair. The histone chaperone Anti-Silencing Factor 1 (ASF1) plays a central role in facilitating CAF-1-mediated replication-dependent H3.1 deposition and HIRA-mediated replication-independent H3.3 deposition in yeast and metazoans. Whether ASF1 function is evolutionarily conserved in plants is unknown. Here, we show that Arabidopsis ASF1 proteins display an exclusive preference for the H3.3-depositing HIRA complex. Simultaneous mutation of both Arabidopsis ASF1 genes caused a decrease in chromatin density and ectopic H3.1 occupancy at loci typically enriched with H3.3. Genetic, transcriptomic, and proteomic data indicate that ASF1 proteins strongly prefer the HIRA complex over CAF-1. asf1 mutants also displayed an increase in spurious Pol II transcriptional initiation, and showed defects in the maintenance of gene body CG DNA methylation and in the distribution of histone modifications. Furthermore, ectopic targeting of ASF1 caused excessive histone deposition, less accessible chromatin, and gene silencing. These findings reveal the importance of ASF1-mediated H3.3-H4 deposition via the HIRA pathway for proper epigenetic regulation of the genome.

2022-10-31 | PXD035578 | Pride

Quantitative middle-down MS analysis of histone H3 proteoforms throughout lifespan in mice

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

Dynamic Deposition of the Histone H3.3 Variant Accompanies Developmental Remodeling of Arabidopsis Transcriptome (mRNA-Seq)

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

Dynamic Deposition of the Histone H3.3 Variant Accompanies Developmental Remodeling of Arabidopsis Transcriptome (ChIP-Seq)

2012-05-15 | E-GEOD-36629 | biostudies-arrayexpress

Dynamic Deposition of the Histone H3.3 Variant Accompanies Developmental Remodeling of Arabidopsis Transcriptome

Project description:This SuperSeries is composed of the following subset Series: GSE36626: Dynamic Deposition of the Histone H3.3 Variant Accompanies Developmental Remodeling of Arabidopsis Transcriptome (mRNA-Seq) GSE36629: Dynamic Deposition of the Histone H3.3 Variant Accompanies Developmental Remodeling of Arabidopsis Transcriptome (ChIP-Seq) Refer to individual Series

2012-05-15 | E-GEOD-36631 | biostudies-arrayexpress

Histone chaperone HIRA orchestrates H4K16ac-decorated dynamic chromatin in senescent cells and is required for suppression of oncogene-induced neoplasia.

Project description:Cellular senescence is a stable proliferation arrest that suppresses tumorigenesis. Histone chaperone HIRA deposits nucleosome-destabilizing histone variant H3.3 into chromatin in a DNA replication-independent manner. Histone H3.3 and a subset of other typically M-bM-^@M-^\replication-dependentM-bM-^@M-^] core histones were expressed in non-proliferating senescent cells, the latter linked to alternative mRNA splicing and polyadenylation. Senescent cells incorporated newly-synthesized histones into chromatin, partially dependent on HIRA. HIRA and newly-deposited histone H3.3 co-localized at promoters of expressed genes, and their distribution shifted between proliferating and senescent cells, paralleling changes in gene expression. In senescent cells, gene promoters showed exceptional enrichment of a histone acetylation linked to open and dynamic chromatin, H4K16ac. Abundance of H4K16ac depended on HIRA. In the mouse, inactivation of HIRA downregulated H4K16ac and dramatically enhanced oncogene-induced hyperplasia. To conclude, HIRA controls a previously undefined dynamic non-canonical H4K16ac-decorated chromatin landscape in senescence, and also plays an unanticipated role in suppression of oncogene-induced neoplasia. Examination of HIRA protein binding alongside histone modification H4K16ac and H3.3 in proliferating and senescent IMR90 cells

2014-11-26 | E-GEOD-56307 | biostudies-arrayexpress

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