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Impaired gene expression in ATRX-depleted cells following interferon signaling

ABSTRACT: We investigated the role of the chromatin remodeling protein ATRX on ISG expression upon stimulation with IFN-β utilizing doxycycline-inducible ATRX knockdown cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE194396 | GEO | 2022/08/03

REPOSITORIES: GEO

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Alterations in chromatin accessibility in ATRX-depleted cells following interferon signaling

Project description:We investigated the role of the chromatin remodeling protein ATRX on chromatin accessibility specifically upon IFN-β stimulation utilizing stable ATRX knockdown cells.

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Impaired gene expression in ATRX-depleted cells following interferon signaling

Project description:Impaired gene expression in ATRX-depleted cells following interferon signaling

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Alterations in chromatin accessibility in ATRX-depleted cells following interferon signaling

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Differential contributions of interferon classes to driving host inflammatory responses and restricting virus progeny production

Project description:The cornerstone of mammalian intrinsic and innate immune defense against pathogens is the production of interferons (IFN), cytokines that stimulate anti-pathogen signaling pathways through the simultaneous expression of hundreds of interferon-stimulated genes (ISG). We compared the effects of IFN classes on the cellular proteome and relative restriction of virus progeny production across multiple physiologically relevant cell types and viruses. We integrated global proteome analyses with targeted mass spectrometry (MS), thermal proximity coaggregation-MS (TPCA-MS), and molecular virology assays to determine how ISGs differentially contribute to host antiviral capacities between immune-modulatory cell types. In differentiated macrophage-like monocytic cells, we classified sets of both shared and distinct ISG proteins responsive to each IFN class. We orthogonally confirmed the relative protein alterations using parallel reaction monitoring (PRM) by developing a proteotypic peptide library for ISG markers induced by each IFN class. Additional comparison to stimulation with pro-inflammatory LPS helped to contextualize the observed IFN signatures. We further assessed ISG protein interactions upon IFN types I and II stimulation, observing maintenance of key ISG protein complexes across treatments. Subsequent comparison of macrophage-like monocytic cells to primary keratinocytes enabled us to identify relative ISG abundances, cytokine induction, and antiviral capacities of both cell types across infections with several ubiquitous human viruses. Infections with herpes simplex virus-1 (HSV-1), adenovirus (AdV), and human cytomegalovirus (HCMV) revealed cell type-dependent differences in virus progeny production.

2024-02-28 | PXD046976 | Pride

Quantitative Analysis of Telomeric Nucleosomal Compaction following ATRX Depletion

Project description:The goal of this experiment is to determine the effect of ATRX depletion on telomeric chromatin compaction. We adapted the ATAC-seq to quantify telomere chromatin accessibility. By scoring the ratio of sequence reads that contained 3 - 12 tandem telomeric repeats over the total number of reads in wild-type and ATRX deplted cells, our analysis revealed that CRISPR/Cas9-mediated ATRX depletion induces a progressive telomere de-compaction.

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Epigenomic analysis of Atrx deficiency in murine glioma cells of orgin [Atrx ChIP]

Project description:The chromatin regulator ATRX is inactivated in large subsets of adult and pediatric glioma. Whether and how ATRX deficiency promotes oncogenesis by epigenomic dysregulation remains unclear. We found that Atrx loss, especially when coupled with Tp53 inactivation, promoted cell motility and modulated differentiation state in primary murine neuroepithelial progenitors, recapitulating characteristic disease phenotypes and molecular features. Moreover, Atrx deficiency induced widespread shifts in chromatin accessibility, histone composition, and gene transcription at vacant Atrx binding sites distributed across the genome. Finally, target genes mediating Atrx-deficient phenotypes in vitro exhibited similarly selective misexpression in ATRX-mutant human glioma tissues and cell lines. These findings demonstrate that, in appropriate physiological contexts, ATRX deficiency and its epigenomic sequelae are sufficient to induce disease-defining oncogenic phenotypes.

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Mapping RNA interactions of human ATRX with RepA fragment of Xist

Project description:Heterochromatin in the eukaryotic genome is rigorously controlled by the concerted action of protein factors and RNAs. Here, we investigate the RNA binding function of ATRX, a chromatin remodeler with roles in silencing of repetitive regions of the genome and in recruitment of the polycomb repressive complex 2 (PRC2). We identify ATRX RNA binding regions (RBRs) and discover that the major ATRX RBR lies within the N-terminal region of the protein, distinct from its PHD and helicase domains. Deletion of this ATRX RBR (ATRXRBR) compromises ATRX interactions with RNAs in vitro and in vivo and alters its chromatin binding properties. Genome-wide studies reveal that loss of RNA interactions results in a redistribution of ATRX on chromatin. Finally, our studies identify a role for ATRX-RNA interactions in regulating PRC2 localization to a subset of polycomb target genes.

2020-03-09 | PXD017806 | Pride

Histone H3 lysine 9 di-methylation as an epigenetic signature of the interferon response (sequencing)

Project description:Effective anti-viral immunity depends on the ability of infected cells or cells triggered with virus-derived nucleic acids to produce type I interferon (IFN), which activates transcription of numerous antiviral genes. However, disproportionately strong or chronic IFN expression is a common cause of inflammatory and autoimmune diseases. Here we describe an epigenetic mechanism that determines cell-type specific differences in IFN and IFN-stimulated gene expression in response to exogenous signals. We identify di-methylation of histone H3 at lysine 9 (H3K9me2) as a suppressor of IFN and IFN-inducible antiviral gene expression. We show that levels of H3K9me2 at IFN and IFN stimulated genes (ISG) correlate inversely with the scope and amplitude of IFN and ISG expression in fibroblasts and dendritic cells. Accordingly, genetic ablation or pharmacological inactivation of lysine methyltransferase G9a, which is essential for the generation of H3K9me2, resulted in phenotypic conversion of fibroblasts into highly potent IFN-producing cells and rendered these cells resistant to pathogenic RNA viruses. In summary, our studies implicate H3K9me2 and enzymes controlling its abundance as key regulators of innate antiviral immunity. Examination of epigenetic modifications in WT and G9a deficient MEFs and splenic DCs

2012-03-02 | E-GEOD-22102 | biostudies-arrayexpress

Examining the role of ATRX-RNA interactions in ATRX and PRC2 localization and gene expression.

Project description:We disrupted the RNA binding region in endogenous ATRX and tested localization of ATRX, EZH2 and H3K27me3 by CUT&RUN. We show that ATRX-RNA binding is important to regulate ATRX and PRC2 localization to specific genes.

2020-02-24 | GSE130452 | GEO

Histone H3 lysine 9 di-methylation as an epigenetic signature of the interferon response (WT and G9a deficient DCs)

Project description:Effective anti-viral immunity depends on the ability of infected cells or cells triggered with virus-derived nucleic acids to produce type I interferon (IFN), which activates transcription of numerous antiviral genes. However, disproportionately strong or chronic IFN expression is a common cause of inflammatory and autoimmune diseases. Here we describe an epigenetic mechanism that determines cell-type specific differences in IFN and IFN-stimulated gene expression in response to exogenous signals. We identify di-methylation of histone H3 at lysine 9 (H3K9me2) as a suppressor of IFN and IFN-inducible antiviral gene expression. We show that levels of H3K9me2 at IFN and IFN stimulated genes (ISG) correlate inversely with the scope and amplitude of IFN and ISG expression in fibroblasts and dendritic cells. Accordingly, genetic ablation or pharmacological inactivation of lysine methyltransferase G9a, which is essential for the generation of H3K9me2, resulted in phenotypic conversion of fibroblasts into highly potent IFN-producing cells and rendered these cells resistant to pathogenic RNA viruses. In summary, our studies implicate H3K9me2 and enzymes controlling its abundance as key regulators of innate antiviral immunity. Examination of gene expression in response to PolyI:C in WT and G9a deficient DCs

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