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Transcription-driven cohesin accumulation is associated with secretory phenotype of senescence [HiC]

ABSTRACT: Transcription-driven cohesin accumulation is associated with secretory phenotype of senescence [HiC]

PROVIDER: PRJNA557420 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9861000_1.fastq.gz	Fastqsanger.gz
	SRR9861000_2.fastq.gz	Fastqsanger.gz
	SRR9861010_1.fastq.gz	Fastqsanger.gz
	SRR9861010_2.fastq.gz	Fastqsanger.gz
	SRR9861001_1.fastq.gz	Fastqsanger.gz

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Transcription-driven cohesin accumulation is associated with secretory phenotype of senescence [HiC]

Project description:Senescence is a stable form of cell cycle arrest that is triggered in response to various pathophysiological stimuli. The three-dimensional structure of senescent cells has been previously characterised, mostly in terms of macro-domains or changes between large heterochromatic regions. In the present body of work, using a combination of HiC and targetted Capture Hi-C, we aimed to investigate the association between gene expression and local chromatin structure in senescence, particularly focusing on enhancer-promoter (EP) interactions. We show that many EP contacts are rewired in RAS-induced Senescence compared to ‘normal’, growing cells and that these are associated with cohesin binding changes and possible loop re-organisation. The genes affected by altered chromatin interactions correspond to the two main axes of senescence gene regulation: cell cycle and inflammation. Our findings are potentially relevant during ageing and in cancers with cohesin mutations, where cell cycle and inflammation are also deregulated.

2020-10-05 | GSE135090 | GEO

Transcription-driven cohesin accumulation is associated with secretory phenotype of senescence

Project description:Transcription-driven cohesin accumulation is associated with secretory phenotype of senescence

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Transcription-driven cohesin accumulation is associated with secretory phenotype of senescence [ChIP-Seq]

Project description:Transcription-driven cohesin accumulation is associated with secretory phenotype of senescence [ChIP-Seq]

| PRJNA557423 | ENA

Transcription-driven cohesin accumulation is associated with secretory phenotype of senescence [ChIP-Seq]

2020-10-05 | GSE135088 | GEO

Iron accumulation drives fibrosis, senescence, and the senescence-associated secretory phenotype

Project description:Iron accumulation drives fibrosis, senescence, and the senescence-associated secretory phenotype

| PRJEB62753 | ENA

Iron accumulation drives fibrosis, senescence, and the senescence-associated secretory phenotype

Project description:We found histological evidence for increased abundance of iron accumulating cells in association with fibrotic lung, kidney, and heart diseases in mice and humans. We showed that inducing iron accumulation by intratracheal iron delivery in mice is a potent inducer of inflammation, cellular senescence, and fibrosis. The aim of this study has been to understand the single cell dynamics of iron accumulation and the mechanics that link it to in vivo senescence and to fibrogenesis. To get deeper insight into how different cell types respond to iron accumulation, we performed single nuclei RNA sequencing (snRNA-seq) of lungs from mice which received a single intratracheal dose of iron 2 or 6 days prior to analysis, or PBS 6days prior to analysis (control).

2023-08-18 | E-MTAB-13032 | biostudies-arrayexpress

Transcription-driven cohesin accumulation is associated with secretory phenotype of senescence

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

2020-10-05 | GSE135093 | GEO

Cohesin loss eliminates all loop domains [HiC]

Project description:Cohesin loss eliminates all loop domains [HiC]

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ADAM19 Mediates Cellular Senescence and the Senescence-Associated Secretory Phenotype

Project description:ADAM19 Mediates Cellular Senescence and the Senescence-Associated Secretory Phenotype

2020-04-03 | MSV000085224 | MassIVE

Branched-Chain Amino Acid Accumulation Fuels the Senescence-Associated Secretory Phenotype.

Project description:The essential branched-chain amino acids (BCAAs) leucine, isoleucine, and valine play critical roles in protein synthesis and energy metabolism. Despite their widespread use as nutritional supplements, BCAAs' full effects on mammalian physiology remain uncertain due to the complexities of BCAA metabolic regulation. Here a novel mechanism linking intrinsic alterations in BCAA metabolism is identified to cellular senescence and the senescence-associated secretory phenotype (SASP), both of which contribute to organismal aging and inflammation-related diseases. Altered BCAA metabolism driving the SASP is mediated by robust activation of the BCAA transporters Solute Carrier Family 6 Members 14 and 15 as well as downregulation of the catabolic enzyme BCAA transaminase 1 during onset of cellular senescence, leading to highly elevated intracellular BCAA levels in senescent cells. This, in turn, activates the mammalian target of rapamycin complex 1 (mTORC1) to establish the full SASP program. Transgenic Drosophila models further indicate that orthologous BCAA regulators are involved in the induction of cellular senescence and age-related phenotypes in flies, suggesting evolutionary conservation of this metabolic pathway during aging. Finally, experimentally blocking BCAA accumulation attenuates the inflammatory response in a mouse senescence model, highlighting the therapeutic potential of modulating BCAA metabolism for the treatment of age-related and inflammatory diseases.

| S-EPMC10787106 | biostudies-literature

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