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High Resolution Mapping of H1 Linker Histone Variants in Embryonic Stem Cells

ABSTRACT: H1 linker histones facilitate higher order chromatin folding and are essential for mammalian development. To achieve high resolution mapping of H1 variants H1d and H1c in embryonic stem cells (ESCs), we have established a knock-in system and shown that the N-terminally tagged H1 proteins are functionally interchangeable to their endogenous counterparts in vivo. H1d and H1c are depleted from GC- and gene-rich regions and active promoters, inversely correlated with H3K4me3, but positively correlated with H3K9me3 and associated with characteristic sequence features. Surprisingly, both H1d and H1c are significantly enriched at major satellites, which display increased nucleosome spacing compared with bulk chromatin. While also depleted at active promoters and enriched at major satellites, overexpressed H10 displays differential binding patterns in specific repetitive sequences compared with H1d and H1c. Depletion of H1c, H1d and H1e causes pericentric chromocenter clustering and de-repression of major satellites. These results integrate the localization of an understudied type of chromatin proteins, namely the H1 variants, into the epigenome map of mouse ESCs, and we identify significant changes at pericentric heterochromatin upon depletion of this epigenetic mark. Mapping linker histone H1 variants H1d, H1c and H10 as well as 3 core histone modifications in mouse ESC genome.

ORGANISM(S): Mus musculus

SUBMITTER: Yuhong Fan

PROVIDER: E-GEOD-46134 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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High Resolution Mapping of H1 Linker Histone Variants in Embryonic Stem Cells

Project description:H1 linker histones facilitate higher order chromatin folding and are essential for mammalian development. To achieve high resolution mapping of H1 variants H1d and H1c in embryonic stem cells (ESCs), we have established a knock-in system and shown that the N-terminally tagged H1 proteins are functionally interchangeable to their endogenous counterparts in vivo. H1d and H1c are depleted from GC- and gene-rich regions and active promoters, inversely correlated with H3K4me3, but positively correlated with H3K9me3 and associated with characteristic sequence features. Surprisingly, both H1d and H1c are significantly enriched at major satellites, which display increased nucleosome spacing compared with bulk chromatin. While also depleted at active promoters and enriched at major satellites, overexpressed H10 displays differential binding patterns in specific repetitive sequences compared with H1d and H1c. Depletion of H1c, H1d and H1e causes pericentric chromocenter clustering and de-repression of major satellites. These results integrate the localization of an understudied type of chromatin proteins, namely the H1 variants, into the epigenome map of mouse ESCs, and we identify significant changes at pericentric heterochromatin upon depletion of this epigenetic mark.

2013-04-29 | GSE46134 | GEO

Analysis of genomic distribution of three linker histone variants in Arabidopsis under normal and low light conditions, by ChIP-chip.

Project description:Linker histones (H1s) are conserved and ubiquitous structural components of eukaryotic chromatin. Multiple non-allelic variants of H1 co-exist in animals and plants, differ in their DNA/nucleosome binding properties and have been implicated in the control of genetic programs during development and differentiation. To study the genome-wide distribution of Arabidopsis H1 variants, ChIP-on-chip technology was used .

2015-07-29 | E-MTAB-2804 | biostudies-arrayexpress

LncRNA SNHG8d impedes chromatin condensation and epithelial differentiation by phase separating histone H1 [RNA-seq]

Project description:Linker histone H1, the key chromatin structural protein facilitating higher order chromatin folding, isan important epigenetic mark and regulator for gene expression and cellular differentiation. However, mechanisms thatregulate H1 binding affinity to chromatin remain elusive. In an attempt to screen functionallong non-coding RNAs(lncRNAs), we designed a cell-type specific score (CTSS) algorithm on the basis of RNA-seq data derived fromcell lines of different origins, which leads to the identification of an epithelium-specific lncRNA designated assmall nucleolar RNA host gene 8 (SNHG8). In epithelial cells, loss of SNHG8d, a major transcriptof SNHG8, remodels the genomic expression profiletowards differentiation. Mechanistically, SNHG8d is localized in the nucleus and manifests stronginteraction withallthe histone H1 variants detected.Loss of SNHG8dleads to increasedH1 binding affinity to chromatinand subsequentchromatin condensationwhichdictates the epithelial differentiation-orientedgenomic expression remodeling.Further analysis proposes that SNHG8d regulates H1-chromatin affinityby competing with linker DNA forhistone H1 binding througha phase-separation mechanism. Thus, our study revealed a lncRNA-conducted mechanismthat sequesters histone H1 from chromatin through phase separation to sequentially regulatechromatin structure, gene expressionandepithelialdifferentiation.

2021-12-31 | GSE151625 | GEO

LncRNA SNHG8d impedes chromatin condensation and epithelial differentiation by phase separating histone H1 [ATAC-seq]

Project description:Linker histone H1, the key chromatin structural protein facilitating higher order chromatin folding, is an important epigenetic mark and regulator for gene expression and cellular differentiation. However, mechanisms thatregulate H1 binding affinity to chromatin remain elusive. In an attempt to screen functionallong non-coding RNAs(lncRNAs), we designed a cell-type specific score (CTSS) algorithm on the basis of RNA-seq data derived fromcell lines of different origins, which leads to the identification of an epithelium-specific lncRNA designated assmall nucleolar RNA host gene 8 (SNHG8). In epithelial cells, loss of SNHG8d, a major transcriptof SNHG8, remodels the genomic expression profiletowards differentiation. Mechanistically, SNHG8d is localized in the nucleus and manifests stronginteraction withallthe histone H1 variants detected.Loss of SNHG8dleads to increasedH1 binding affinity to chromatinand subsequentchromatin condensationwhichdictates the epithelial differentiation-orientedgenomic expression remodeling.Further analysis proposes that SNHG8d regulates H1-chromatin affinityby competing with linker DNA forhistone H1 binding througha phase-separation mechanism. Thus, our study revealed a lncRNA-conducted mechanismthat sequesters histone H1 from chromatin through phase separation to sequentially regulatechromatin structure, gene expressionandepithelialdifferentiation.

2021-12-31 | GSE151624 | GEO

Mapping of somatic linker histone H1 variants in T47D-MTVL and HeLa cells

Project description:At least six histone H1 variants exist in mammalian somatic cells that bind to the linker DNA and stabilize the nucleosome particle contributing to higher order chromatin compaction. In addition, H1 seems to be involved in the active regulation of gene expression. It is not well known whether the different variants have specific roles, are distributed differentially along the genome, or regulate specific promoters. By taking advantage of specific antibodies to H1 variants and HA-tagged recombinant H1 variants expressed in a breast cancer-derived cell line, we have investigated the distribution of the different somatic H1 variants (H1.2 to H1.5, H1.0 and H1X) in particular promoters and genome-wide. Analysis of H1 (H1.0, H1.2, H1.3, H1.4, H1.5 and H1X) and H3 abundance in promoter regions

2014-02-04 | E-GEOD-49333 | biostudies-arrayexpress

Mapping of somatic linker histone H1 variants in T47D-MTVL cells

Project description:At least six histone H1 variants exist in mammalian somatic cells that bind to the linker DNA and stabilize the nucleosome particle contributing to higher order chromatin compaction. In addition, H1 seems to be involved in the active regulation of gene expression. It is not well known whether the different variants have specific roles, are distributed differentially along the genome, or regulate specific promoters. By taking advantage of specific antibodies to H1 variants and HA-tagged recombinant H1 variants expressed in a breast cancer-derived cell line, we have investigated the distribution of the different somatic H1 variants (H1.2 to H1.5, H1.0 and H1X) in particular promoters and genome-wide. Genome-wide analysis of H1.0, H1.2, H1.4, H1X and H3

2014-02-04 | E-GEOD-49334 | biostudies-arrayexpress

Mapping of somatic linker histone H1 variants in T47D-MTVL cells

2014-02-04 | GSE49334 | GEO

Mapping of somatic linker histone H1 variants in T47D-MTVL and HeLa cells

2014-02-04 | GSE49333 | GEO

Gene expression in response to depletion of specific human histone H1 isoforms.

Project description:At least six histone H1 variants exist in mammalian somatic cells that bind to the linker DNA and stabilize the nucleosome particle contributing to higher order chromatin compaction. In addition, H1 seems to be involved in the active regulation of gene expression. It is not well known whether the different variants have specific roles or regulate specific promoters. We have explored this by inducible shRNA-mediated knock-down of each of the H1 variants in a human breast cancer cell line. A different subset of genes is altered in each H1 knock-down. Keywords: cell type comparison; genetic modification; RNA interference

2008-10-20 | GSE12299 | GEO

The genomic landscape of the somatic linker histone subtypes H1.1 to H1.5 in human cells

Project description:We employed the DamID technique to systematically map the genomic distribution of all canonical somatic H1 subtypes (H1.1-H1.5) in human IMR90 cells. Human cells contain up to eleven histone H1 proteins, with different spatial and temporal expression patterns. These include five canonical, replication-dependent somatic H1 subtypes (H1.1, H1.2, H1.3, H1.4 and H1.5). Despite being a key chromatin component, the genomic distribution of the somatic canonical H1 subtypes is still unknown and their role in chromatin related processes has so far remained elusive. Here we employed a DamID approach to map for the first time the genomic localization of all somatic canonical H1 subtypes in human cells. Our integrative analysis reveals novel insights into H1 subtype distribution and uncovers functional chromatin features potentially regulating the H1 genomic landscape. In general H1.2 to H1.5 are depleted from GC-rich regions and regulatory regions associated with active transcription. H1.1 shows a binding profile distinct from the other subtypes, suggesting a unique function for H1.1 in chromatin-regulated processes. Interestingly, our data indicate a novel role for somatic H1 subtypes in the three-dimensional organization of the genome by marking repressive regions within topological domains such as LADs. Our work integrates the five somatic linker histone H1 subtypes into the epigenome maps of human cells and provides a resource to refine our understanding of the significance of H1 and its heterogeneity in the control of genome function. DamID profiling of somatic linker histone variants H1.1, H1.2, H1.3, H1.4 and H1.5 in human fibroblasts. Two biological replicate samples of all H1 variants were hybridized on NimbleGen Human ChIP-chip 2.1M Economy Whole-Genome Tiling - Array GPL16055 covering small human chromosomes.

2013-06-15 | E-GEOD-40886 | biostudies-arrayexpress

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