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NOTCH-mediated non-cell autonomous regulation of chromatin structure during senescence

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE103590 | GEO | 2018/04/24

REPOSITORIES: GEO

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NOTCH-mediated non-cell autonomous regulation of chromatin structure during senescence.

Project description:Senescent cells interact with the surrounding microenvironment achieving diverse functional outcomes. We have recently identified that NOTCH1 can drive 'lateral induction' of a unique senescence phenotype in adjacent cells by specifically upregulating the NOTCH ligand JAG1. Here we show that NOTCH signalling can modulate chromatin structure autonomously and non-autonomously. In addition to senescence-associated heterochromatic foci (SAHF), oncogenic RAS-induced senescent (RIS) cells exhibit a massive increase in chromatin accessibility. NOTCH signalling suppresses SAHF and increased chromatin accessibility in this context. Strikingly, NOTCH-induced senescent cells, or cancer cells with high JAG1 expression, drive similar chromatin architectural changes in adjacent cells through cell-cell contact. Mechanistically, we show that NOTCH signalling represses the chromatin architectural protein HMGA1, an association found in multiple human cancers. Thus, HMGA1 is involved not only in SAHFs but also in RIS-driven chromatin accessibility. In conclusion, this study identifies that the JAG1-NOTCH-HMGA1 axis mediates the juxtacrine regulation of chromatin architecture.

| S-EPMC5943456 | biostudies-literature

NOTCH-mediated non-cell autonomous regulation of chromatin structure during senescence [ChIP-Seq]

Project description:We describe the accessible chormatin landscape in RAS-induced (RIS) and NOTCH induced senescence (NIS) using ATAC-seq. By expressing active NOTCH (N1ICD) in the context of RIS, we find that N1ICD antagonizes the formation of accessible regions in RIS. By performing co-cultures, we demonstrate that cells expressing a NOTCH1 ligand, JAGGED1, can antagonize the formation of RIS specific accessible regions. Many of these accessible regions form at enhancers, characterised using ChIP-seq against H3K4me1 and H3K27Ac

2018-04-24 | GSE103589 | GEO

NOTCH-mediated non-cell autonomous regulation of chromatin structure during senescence [ATAC-Seq]

2018-04-24 | GSE103588 | GEO

NOTCH-mediated non-cell autonomous regulation of chromatin structure during senescence [RNA-Seq]

Project description:We decribe the accessible chormatin landscape in RAS-induced (RIS) and NOTCH induced senescence (NIS) using ATAC-seq. By expressing active NOTCH (N1ICD) in the context of RIS, we find that N1ICD antagonises the formation of accessible regions in RIS. By performing co-cultures, we demonstrate that cells expressing a NOTCH1 ligand, JAGGED1, can antagonise the formation of RIS specific accessible regions.

2018-04-24 | GSE113060 | GEO

NOTCH-mediated non-cell autonomous regulation of chromatin structure during senescence

Project description:NOTCH-mediated non-cell autonomous regulation of chromatin structure during senescence

| PRJNA402006 | ENA

NOTCH-mediated non-cell autonomous regulation of chromatin structure during senescence [RNA-Seq]

Project description:NOTCH-mediated non-cell autonomous regulation of chromatin structure during senescence [RNA-Seq]

| PRJNA449912 | ENA

METTL3-mediated chromatin contacts promote phase separation during senescence.

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

2024-04-22 | GSE243047 | GEO

Lysosome-mediated processing of chromatin in senescence.

Project description:Cellular senescence is a stable proliferation arrest, a potent tumor suppressor mechanism, and a likely contributor to tissue aging. Cellular senescence involves extensive cellular remodeling, including of chromatin structure. Autophagy and lysosomes are important for recycling of cellular constituents and cell remodeling. Here we show that an autophagy/lysosomal pathway processes chromatin in senescent cells. In senescent cells, lamin A/C-negative, but strongly γ-H2AX-positive and H3K27me3-positive, cytoplasmic chromatin fragments (CCFs) budded off nuclei, and this was associated with lamin B1 down-regulation and the loss of nuclear envelope integrity. In the cytoplasm, CCFs were targeted by the autophagy machinery. Senescent cells exhibited markers of lysosomal-mediated proteolytic processing of histones and were progressively depleted of total histone content in a lysosome-dependent manner. In vivo, depletion of histones correlated with nevus maturation, an established histopathologic parameter associated with proliferation arrest and clinical benignancy. We conclude that senescent cells process their chromatin via an autophagy/lysosomal pathway and that this might contribute to stability of senescence and tumor suppression.

| S-EPMC3704985 | biostudies-literature

Chromosomal instability-induced senescence potentiates cell non-autonomous tumourigenic effects.

Project description:Chromosomal instability (CIN), a high rate of chromosome loss or gain, is often associated with poor prognosis and drug resistance in cancers. Aneuploid, including near-polyploid, cells contain an abnormal number of chromosomes and exhibit CIN. The post-mitotic cell fates following generation of different degrees of chromosome mis-segregation and aneuploidy are unclear. Here we used aneuploidy inducers, nocodazole and reversine, to create different levels of aneuploidy. A higher extent of aneuploid and near-polyploid cells in a given population led to senescence. This was in contrast to cells with relatively lower levels of abnormal ploidy that continued to proliferate. Our findings revealed that senescence was accompanied by DNA damage and robust p53 activation. These senescent cells acquired the senescence-associated secretory phenotype (SASP). Depletion of p53 reduced the number of senescent cells with concomitant increase in cells undergoing DNA replication. Characterisation of these SASP factors demonstrated that they conferred paracrine pro-tumourigenic effects such as invasion, migration and angiogenesis both in vitro and in vivo. Finally, a correlation between increased aneuploidy and senescence was observed at the invasive front in breast carcinomas. Our findings demonstrate functional non-equivalence of discernable aneuploidies on tumourigenesis and suggest a cell non-autonomous mechanism by which aneuploidy-induced senescent cells and SASP can affect the tumour microenvironment to promote tumour progression.

| S-EPMC6092349 | biostudies-literature

Non-cell-autonomous regulation of interneuron specification mediated by extracellular vesicles

Project description:We performed RNA-seq analysis on neural progenitor cells (NPCs) acutely treated (12 hours) with Extracellular vesicles (EVs) purified by the conditioned medium of dorsally patterned and ventrally patterned human cerebral organoids originated from control- or E370K mutant- iPSCs cells. The aim of this experiments was to dissect if EV content leads to transcriptional changes on receiving cells.

2023-06-23 | GSE197252 | GEO

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