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H3K9 trimethylation in active compartments optimizes stimulus-regulated transcription by restricting usage of CTCF sites in SINE-B2 repeats

ABSTRACT: H3K9 trimethylation in active compartments optimizes stimulus-regulated transcription by restricting usage of CTCF sites in SINE-B2 repeats

PROVIDER: PRJNA785450 | ENA |

REPOSITORIES: ENA

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H3K9 trimethylation in active compartments optimizes stimulus-regulated transcription by restricting usage of CTCF sites in SINE-B2 repeats [HiC]

Project description:H3K9 trimethylation in active compartments optimizes stimulus-regulated transcription by restricting usage of CTCF sites in SINE-B2 repeats [HiC]

| PRJNA785445 | ENA

H3K9 trimethylation in active compartments optimizes stimulus-regulated transcription by restricting usage of CTCF sites in SINE-B2 repeats [HiC]

Project description:Six methyltransferases divide labor in establishing genomic profiles of histone H3 lysine 9 methylation (H3K9me), an epigenomic modification involved in the formation of constitutive heterochromatin, gene repression and silencing of retroelements. Among them, SETDB1 is recruited to active chromatin compartments to silence the expression of endogenous retroviruses. In the context of experiments aimed at determining the role of SETDB1 in stimulus-inducible gene expression in macrophages, we unexpectedly found that upon SETDB1 depletion, loss of H3K9me3 in active compartments was associated with increased recruitment of CTCF to >1,600 DNA-binding motifs contained within SINE-B2 repeats, a previously unidentified target of SETDB1-mediated repression. CTCF is an essential regulator of chromatin folding that restrains DNA looping by cohesin, thus creating boundaries among adjacent topological domains. Increased CTCF binding to SINE-B2 repeats generated novel boundaries within topological domains containing lipopolysaccharide-inducible genes, correlating with their impaired regulation in response to stimulation. These data indicate a role of H3K9me3 in restraining genomic distribution and activity of CTCF, with impact on chromatin organization and gene regulation.

2022-03-31 | GSE189973 | GEO

H3K9 trimethylation in active compartments optimizes stimulus-regulated transcription by restricting usage of CTCF sites in SINE-B2 repeats [RNA-Seq]

2022-03-31 | GSE189974 | GEO

H3K9 trimethylation in active compartments optimizes stimulus-regulated transcription by restricting usage of CTCF sites in SINE-B2 repeats [ChIP-Seq]

2022-03-31 | GSE189971 | GEO

H3K9 trimethylation in active compartments optimizes stimulus-regulated transcription by restricting usage of CTCF sites in SINE-B2 repeats [ATAC-Seq]

2022-03-31 | GSE189970 | GEO

H3K9 trimethylation in active compartments optimizes stimulus-regulated transcription by restricting usage of CTCF sites in SINE-B2 repeats [ChIP-Seq]

Project description:H3K9 trimethylation in active compartments optimizes stimulus-regulated transcription by restricting usage of CTCF sites in SINE-B2 repeats [ChIP-Seq]

| PRJNA785447 | ENA

H3K9 trimethylation in active compartments optimizes stimulus-regulated transcription by restricting usage of CTCF sites in SINE-B2 repeats [RNA-Seq]

Project description:H3K9 trimethylation in active compartments optimizes stimulus-regulated transcription by restricting usage of CTCF sites in SINE-B2 repeats [RNA-Seq]

| PRJNA785459 | ENA

H3K9 trimethylation in active compartments optimizes stimulus-regulated transcription by restricting usage of CTCF sites in SINE-B2 repeats [ATAC-Seq]

Project description:H3K9 trimethylation in active compartments optimizes stimulus-regulated transcription by restricting usage of CTCF sites in SINE-B2 repeats [ATAC-Seq]

| PRJNA785448 | ENA

H3K9 trimethylation in active compartments optimizes stimulus-regulated transcription by restricting usage of CTCF sites in SINE-B2 repeats

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-03-31 | GSE189975 | GEO

SINE RNAs trigger noncanonical NLRC4 inflammasome via DDX17

Project description:Short interspersed element (SINE) RNAs are upregulated by cellular stresses1 (heat shock, DNA damage and viral infection) and accumulate in human diseases (macular degeneration2, lupus3, and Alzheimer’s disease4). These transcripts activate inflammasomes5, a family of cytoplasmic multiprotein complexes that sense danger molecules and initiate innate immune responses by activating caspase-1-dependent cytokine production and inflammatory death6, but the molecular sensor of SINE RNAs is unknown. Here, we identify DDX17, a member of the DEAD box family of RNA helicases7, as a sensor of SINE RNAs requisite for inflammasome activation. Induction of caspase-1 cleavage and release of IL-1 and IL-18 by SINE RNAs requires dual recruitment of NLRP3 and NLRC4 but proceeds independent of NAIPs, immune sensors required for canonical NLRC4 activation by bacterial proteins8,9. Instead, SINE RNAs trigger DDX17–NLRC4 interaction, which licenses inflammasome activation. We also report increased levels of DDX17 protein and association of DDX17 and NLRC4 in the retinal pigmented epithelium (RPE) of human eyes with an advanced, untreatable form of age-related macular degeneration (AMD). Disrupting DDX17–NLRC4 signalling blocks SINE RNA-induced inflammasome activation in human RPE cells and RPE degeneration in an animal model of AMD. Our findings uncover a non-canonical mode of inflammasome activation by endogenous retrotransposon transcripts, and provide new potential targets for macular degeneration and potentially other diseases.

2022-06-09 | PXD016019 | Pride

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