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High-resolution Hi-C reveals increased chromatin looping with senescence associated with hypomethylation and retrotransposon derepression [Hi-C]

ABSTRACT: High-resolution Hi-C reveals increased chromatin looping with senescence associated with hypomethylation and retrotransposon derepression [Hi-C]

PROVIDER: PRJNA1117444 | ENA |

REPOSITORIES: ENA

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High-resolution Hi-C reveals increased chromatin looping with senescence associated with hypomethylation and retrotransposon derepression [RNA-seq]

Project description:High-resolution Hi-C reveals increased chromatin looping with senescence associated with hypomethylation and retrotransposon derepression [RNA-seq]

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High-resolution Hi-C reveals increased chromatin looping with senescence associated with hypomethylation and retrotransposon derepression [Long Read DNA-seq]

Project description:High-resolution Hi-C reveals increased chromatin looping with senescence associated with hypomethylation and retrotransposon derepression [Long Read DNA-seq]

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High-resolution Hi-C reveals increased chromatin looping with senescence associated with hypomethylation and retrotransposon derepression [Hi-C]

Project description:This study presents the highest-resolution chromatin map of cellular senescence to date, shedding light on how genomic architecture is altered with this damaging phenotype. Senescence, a driver of aging, is a pro-inflammatory state of proliferative arrest caused by DNA damage; it is associated with epigenetic changes, including those to chromatin organization. We created ~3kb Hi-C contact maps of proliferating, quiescent, and replicative senescent lung fibroblasts, and also compared these to oncogene-induced senescence. Our findings confirm a loss of heterochromatin, with a shift towards the A compartment and A subcompartments. We establish a novel loop analysis framework, revealing the ~six times more unique loops with senescence, which lose methylation at their anchors. Additionally, we present a custom long-read reference genome highlighting structural changes supporting retrotransposon derepression, particularly at a defined ‘hotspot’. These architectural changes contribute to senescence, as they promote cell cycle arrest and inflammation, as well as epigenetic drift.

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Retrotransposon derepression leads to activation of the unfolded protein response and apoptosis in pro B cells

Project description:The establishment of distinct transcription programs during development is controlled by transcription factor networks acting in specific chromatin environments. The H3K9me3-specific histone methyltransferase Setdb1 impacts on transcriptional regulation by repressing both developmental genes and retrotransposons. How impaired retrotransposon silencing may lead to developmental phenotypes is currently unclear. Here we show that loss of Setdb1 in pro-B cells completely abrogates B cell development. In pro-B cells, Setdb1 is dispensable for silencing of lineage-inappropriate developmental genes. Instead, we detect strong derepression of endogenous Murine Leukemia Virus (MLV) copies. Production of MLV proteins leads to activation of the unfolded protein response pathway and apoptosis. Thus, our data demonstrate that B cell development critically depends on the proper repression of retrotransposon sequences through Setdb1. Transcriptomic and chromatin analysis of control and Setdb1-deficient pro-B cells

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