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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.

ORGANISM(S): Mus musculus

PROVIDER: GSE46134 | GEO | 2013/04/29

SECONDARY ACCESSION(S): PRJNA197331

REPOSITORIES: GEO

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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. Mapping linker histone H1 variants H1d, H1c and H10 as well as 3 core histone modifications in mouse ESC genome.

2013-04-29 | E-GEOD-46134 | biostudies-arrayexpress

Transcription profiling of wild type and H1c, H1d, H1e triple null mouse embryonic stem cells to study the effects of loss of the three linker histone subtypes on gene regulation.

Project description:Affymetrix expression profiling of wild-type and H1c, H1d, H1e triple null mouse embryonic stem cells revealed that loss of three linker histone subtypes (H1c, H1d and H1e) results in specific changes in gene regulation. Experiment Overall Design: Affymetrix experiments performed on RNA extracted from wild-type and two H1c/H1d/H1e triple null ES cell lines and data acquired in duplicate.

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Expression data from WT, H1c/H1d/H1e triple null ES cells

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H1 linker histones regulate the balance of repressive and active chromatin domains via localized genomic compaction [ATAC-seq]

Project description:H1 linker histones are the most abundant chromatin binding proteins. Their association with chromatin determines the spacing between nucleosomes and enables arrays of nucleosomes to fold into more compact chromatin structures. Mammals express multiple H1 proteins and are able to compensate for the loss of one or even two members by increasing synthesis of other members to maintain a constant H1 to nucleosome stoichiometry. To study the role of H1 in mammalian development, we generated a conditional triple H1 knockout (H1cTKO) mouse strain that enables depletion of H1 in specific cell types. Here, we report on the effects of depleting H1 in adult hematopoietic cells. Deletion of the genes encoding three widely expressed H1 subtypes (H1c, H1d, and H1e) has particularly profound effects on B- and T- lymphocyte development. H1 depletion leads to de-repression of T-cell activation genes, and a shift in T-cells towards effector functions, a process that mimics normal T-cell activation. Comparison of chromatin structure in normal and H1-depleted CD8+ T-cells revealed that H1 binding produces localized chromatin compaction within spatially defined chromatin domains containing above average levels of H1. Reduction of H1 stoichiometry in these regions leads to decreases in H3K27 methylation and increases in H3K36 methylation. In vitro, H1 promotes PRC2-mediated H3K27 methylation and inhibits NSD2-mediated H3K36 methylation. Mechanistically, H1 mediates these opposite effects by promoting physical compaction of the chromatin substrate. These findings identify H1 as a critical regulator of the epigenetic landscape in mammalian cells.

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H1 linker histones regulate the balance of repressive and active chromatin domains via localized genomic compaction [Hi-C]

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H1 linker histones regulate the balance of repressive and active chromatin domains via localized genomic compaction [CUT&Tag]

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H1 linker histones regulate the balance of repressive and active chromatin domains via localized genomic compaction [RNA-seq]

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H1 linker histones regulate the balance of repressive and active chromatin domains via localized genomic compaction [ChIP-seq]

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Histone 1 deficiency drives lymphomagenesis through disruption of 3D chromatin architecture

Project description:Linker histone H1 proteins bind to nucleosomes and cause chromatin compaction, although little is known about their biological functions. Histone H1 (HIST1H1B-E) mutations are highly recurrent in B-cell lymphomas and are present in solid tumors, but their cancer relevance and mechanism are unknown. Here we report that lymphoma-associated H1 alleles are genetic driver mutations in lymphomas. H1 mutations disrupt their ability to bind or compact chromatin. This causes profound architectural remodeling of the genome characterized by large-scale, yet focal shifts of chromatin from a compacted, to a relaxed state. The degree of decompaction results in distinct epigenetic states, primarily due to gain of histone H3 lysine 36 dimethylation, and/or loss of repressive H3K27 methylation. These changes unlock expression of stem cell genes that are normally silenced during early development. Loss of H1c and H1e alleles in mice conferred enhanced fitness and self renewal properties to germinal center B-cells, ultimately leading to aggressive lymphoma with enhanced repopulating potential. Collectively, our data indicate that H1 proteins are normally required to sequester early developmental genes into architecturally inaccessible genomic compartments. We furthermore establish H1 as a bona fide tumor suppressor, whose mutation drives malignant transformation primarily through three-dimensional genome reorganization, epigenetic reprogramming and aberrant de-repression of developmentally silenced genes.

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