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

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

PROVIDER: PRJNA1117442 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29205888_1.fastq.gz	Fastqsanger.gz
	SRR29205889_1.fastq.gz	Fastqsanger.gz

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

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

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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: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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