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Genomic distribution of linker histone varinat H1T

ABSTRACT: We report genome-wide distribution of germ cell-specific linker histone variant H1T in cancer cell line AGS, MDA-MB-231, and mouse embryonic stem cells (mESCs). We found that H1T expressed not only testis but also non-germ cells such as cancer cells and pluripotent stem cells and showed the biased distribution at rDNA repeat unit. Moreover, on the rDNA region, H1T regulated the chromatin structure and pre-rRNA expression. This study using ChIP-seq analysis provides genomic distribution of H1T in non-germinal cells.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE75287 | GEO | 2016/03/30

SECONDARY ACCESSION(S): PRJNA303106

REPOSITORIES: GEO

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Genomic distribution of linker histone varinat H1T

Project description:We report genome-wide distribution of germ cell-specific linker histone variant H1T in cancer cell line AGS, MDA-MB-231, and mouse embryonic stem cells (mESCs). We found that H1T expressed not only testis but also non-germ cells such as cancer cells and pluripotent stem cells and showed the biased distribution at rDNA repeat unit. Moreover, on the rDNA region, H1T regulated the chromatin structure and pre-rRNA expression. This study using ChIP-seq analysis provides genomic distribution of H1T in non-germinal cells. ChIP-seq analysis of linker histone H1T in AGS, MDA-MB-231 and mESCs

2016-03-30 | E-GEOD-75287 | biostudies-arrayexpress

Dynamic Distribution of Linker Histone H1.5 in Cellular Differentiation

Project description:Linker histones are essential components of chromatin but the distributions and functions of many during cellular differentiation is not well understood. Here, we show that H1.5 binds to genic and intergenic regions, forming blocks of enrichment, in differentiated human cells from all three embryonic germ layers but not in embryonic stem cells. In differentiated cells, H1.5, but not H1.3, binds preferentially to genes that encode membrane and membrane-related proteins. Strikingly, 37% of H1.5 target genes belong to gene family clusters, groups of homologous genes that are located in proximity to each other on chromosomes. H1.5 binding is associated with gene repression and is required for SIRT1 binding, H3K9me2 enrichment and chromatin compaction. Depletion of H1.5 results in loss of SIRT1 and H3K9me2, increased chromatin accessibility, deregulation of gene expression and decreased cell growth. Our data reveal for the first time a specific and novel function for linker histone subtype H1.5 in maintenance of condensed chromatin at defined gene families in differentiated human cells. Examine human linker histone H1.5 (HIST1H1B) binding pattern in H1 hESCs and IMR90 fibroblasts

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Project description:Linker histones are essential components of chromatin but the distributions and functions of many during cellular differentiation is not well understood. Here, we show that H1.5 binds to genic and intergenic regions, forming blocks of enrichment, in differentiated human cells from all three embryonic germ layers but not in embryonic stem cells. In differentiated cells, H1.5, but not H1.3, binds preferentially to genes that encode membrane and membrane-related proteins. Strikingly, 37% of H1.5 target genes belong to gene family clusters, groups of homologous genes that are located in proximity to each other on chromosomes. H1.5 binding is associated with gene repression and is required for SIRT1 binding, H3K9me2 enrichment and chromatin compaction. Depletion of H1.5 results in loss of SIRT1 and H3K9me2, increased chromatin accessibility, deregulation of gene expression and decreased cell growth. Our data reveal for the first time a specific and novel function for linker histone subtype H1.5 in maintenance of condensed chromatin at defined gene families in differentiated human cells. Examine mRNA expression in control and H1.5 knockdown IMR90 cells

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Genomic distribution of linker histone varinat H1T

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Genome Wide Distribution of Linker Histone H1.0 is Independent of MeCP2 II

Project description:Previous studies suggested that MeCP2 binds to linker DNA and competes with linker histone H1 to regulate chromatin structure, but this hypothesis has never been tested in vivo. Here, we expressed Flag-tagged H1.0 in forebrain excitatory neurons in mice and performed ChIP-Seq to reveal H1.0 distribution and its relationship with MeCP2. Unexpectedly, we detected no major change in H1.0 upon MeCP2 depletion, revealing that MeCP2 functions independent of linker H1.0.

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Genome Wide Distribution of Linker Histone H1.0 is Independent of MeCP2 I

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Genomic Binding of Human Linker Histone H1.5 during differentiation (ChIP-chip)

Project description:In humans, there are eleven subtypes of linker histones that exhibit cell- and tissue-specific expression. Linker histone H1 proteins bind to both the core histones and linker DNA of chromatin fibers; and not only participate in control of gene activity but also serve to stabilize higher order chromatin structure. To determine the potential roles of linker histones in differentiation, we examined the global distribution of linker histone subtype H1.5 in human IMR90 fibroblasts and H1 embryonic stem cells (hESCs). Surprisingly, H1.5 binds to and represses a large fraction of gene family clusters in fully differentiated cell types representing all three embryonic germ layers. Little or no H1.5 enrichment at gene family clusters was detected in undifferentiated hESCs or partially differentiated somatic cells. We also found that SIRT1 histone deacetylase and H3K9me2, a repressive histone modification, are also enriched at gene family cluster in IMR90 cells, likely generating a stably repressive chromatin domain. To find out the mechanism of H1.5 targeting, H1.5 or SIRT1 was depleted in IMR90 cells by siRNA, and the binding patterns of SIRT1 and H1.5 were examined. In H1.5 knockdown cells, SIRT1 binding pattern was changed dramatically, and this changed pattern highly correlates to SIRT1 distribution in hESC. However, depletion of SIRT1 could not change the global binding pattern of H1.5. Depletion of H1.5 or SIRT1 leads to up-regulation of ~50% gene family clusters. However, the sets of gene family clusters that are affected by these two factors are different, suggesting H1.5 and SIRT1 may regulate gene transcription via different pathways.

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