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Dynamic Distribution of Linker Histone H1.5 in Cellular Differentiation

ABSTRACT: 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

ORGANISM(S): Homo sapiens

SUBMITTER: Jing-Yu Li

PROVIDER: E-GEOD-26967 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression profile of H1.5 knockdown and SIRT1 knockdown IMR90 cells versus control cells

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. Two-color microarrays. Two replicates for each sample.

2012-09-18 | E-GEOD-26856 | biostudies-arrayexpress

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

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Gene expression profile of H1.5 knockdown and SIRT1 knockdown IMR90 cells versus control cells

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Gene expression profile of H1 human embryonic stem cells, IMR90 lung fibroblasts, calcium induced keratinocytes, and primary hepatocytes

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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 mRNA expression in control and H1.5 knockdown IMR90 cells

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Dynamic Distribution of Linker Histone H1.5 in Cellular Differentiation

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Human Linker Histone H1.5

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2012-12-12 | E-GEOD-26979 | biostudies-arrayexpress

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

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