Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Global decay of regulatory chromatin architecture promotes rebalancing of gene expression during colorectal cancer development [RNA-seq II]

ABSTRACT: Although the 3D genome architecture is essential for long-range gene regulation, the significance of physical chromatin interactions is challenged by recent findings of mutual insensitiveness between contact propensity and gene expression. Here we report hundred basepair-resolution profiling of chromatin conformation in 33 colon tissues tracing the formation and malignant transformation of colorectal polyps. We identified progressive genome-wide decays of chromatin structures such as interaction stripes and loops on all types of cis-regulatory elements, particularly promoters, independent to the alterations of DNA methylation and chromatin accessibility. Instead of linearly correlated with degree of structural decays, transcription levels shifted toward correction of their quantitative mismatching with corresponding promoter contact propensity. These observations suggest increasing sensitivity of transcription to regulatory architecture integrity along with its loss during early cancer development, a mechanism which may provide novel insights to the misregulations of cancer driving genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE255300 | GEO | 2024/02/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Global decay of regulatory chromatin architecture promotes rebalancing of gene expression during colorectal cancer development [RNA-Seq]

Project description:Although the 3D genome architecture is essential for long-range gene regulation, the significance of physical chromatin interactions is challenged by recent findings of mutual insensitiveness between contact propensity and gene expression. Here we report hundred basepair-resolution profiling of chromatin conformation in 33 colon tissues tracing the formation and malignant transformation of colorectal polyps. We identified progressive genome-wide decays of chromatin structures such as interaction stripes and loops on all types of cis-regulatory elements, particularly promoters, independent to the alterations of DNA methylation and chromatin accessibility. Instead of linearly correlated with degree of structural decays, transcription levels shifted toward correction of their quantitative mismatching with corresponding promoter contact propensity. These observations suggest increasing sensitivity of transcription to regulatory architecture integrity along with its loss during early cancer development, a mechanism which may provide novel insights to the misregulations of cancer driving genes.

2022-08-29 | GSE207949 | GEO

Global decay of regulatory chromatin architecture promotes rebalancing of gene expression during colorectal cancer development [Hi-C]

2022-08-29 | GSE207951 | GEO

Global decay of regulatory chromatin architecture promotes rebalancing of gene expression during colorectal cancer development [ATAC-Seq]

2022-08-29 | GSE207950 | GEO

The cohesin acetylation cycle controls chromatin loop length through a PDS5A brake mechanism

Project description:Cohesin structures the genome through the formation of chromatin loops and by holding together the sister chromatids. The acetylation of cohesin’s SMC3 subunit is a dynamic process that involves the acetyltransferase ESCO1 and deacetylase HDAC8. Here we show that this cohesin acetylation cycle controls the 3D genome. ESCO1 restricts the length of chromatin loops and architectural stripes, while HDAC8 promotes the extension of such loops and stripes. This role in controlling loop length turns out to be distinct from the canonical role of cohesin acetylation that protects against WAPL-mediated DNA release. We reveal that acetylation rather controls cohesin’s interaction with PDS5A to restrict chromatin loop length. Our data supports a model in which this PDS5A-bound state acts as a brake that enables the pausing and restart of loop enlargement. The cohesin acetylation cycle hereby provides punctuation in the process of genome folding.

2022-03-14 | PXD032185 | Pride

Subtle changes in chromatin loop contact propensity are associated with differential gene regulation and expression

Project description:Subtle changes in chromatin loop contact propensity are associated with differential gene regulation and expression

| PRJNA516703 | ENA

Proximity-dependent recruitment of Polycomb Repressive Complexes by the lncRNA Airn [Hi-C]

Project description:In the developing mouse embryo, expression of the lncRNA Airn induces gene silencing and recruits Polycomb Repressive Complexes (PRCs) to varying extents over a 15 megabase domain, but the mechanisms remain unclear. Using high-resolution approaches, we show in mouse trophoblast stem cells that Airn expression induces long-range changes to chromatin architecture centered around a network of CpG islands occupied by PRCs and SMC1A/Cohesin. Extent of contact with Airn predicts underlying intensity of Polycomb-directed chromatin modifications and Airn-induced changes to chromatin architecture. Deletion of individual CpG islands alternately increase or decrease gene silencing and PRC activity over the domain in a manner predicted by changes in chromatin architecture. We conclude that Airn is a potent repressive lncRNA whose effects are controlled by an equilibratory network of DNA regulatory elements that modulate its frequency of contact with target chromatin.

2023-07-01 | GSE217823 | GEO

Proximity-dependent recruitment of Polycomb Repressive Complexes by the lncRNA Airn [CHART-Seq]

2023-07-01 | GSE217261 | GEO

Proximity-dependent recruitment of Polycomb Repressive Complexes by the lncRNA Airn [RNA-Seq]

2023-07-01 | GSE217239 | GEO

The energetics and physiological impact of cohesin extrusion

Project description:Cohesin extrusion is thought to play a central role in establishing the architecture of mammalian genomes. However, extrusion has not been visualized in vivo, and thus, its functional impact and energetics are unknown. Using ultra-deep Hi-C, we show that loop domains form by a process that requires cohesin ATPases. Once formed, however, loops and compartments are maintained for hours without energy input. Strikingly, without ATP, we observe the emergence of hundreds of CTCF-independent loops that link regulatory DNA. We also identify architectural "stripes" where a loop anchor interacts with entire domains at high frequency. Stripes often tether super-enhancers to cognate promoters, and in B cells, they facilitate Igh transcription and recombination. Stripe anchors represent major hotspots for topoisomerase-mediated lesions, which promote chromosomal translocations and cancer. In plasmacytomas, stripes can deregulate Igh-translocated oncogenes. We propose that higher organisms have coopted cohesin extrusion to enhance transcription and recombination, with implications for tumor development.

2018-05-01 | GSE98119 | GEO

Subtle changes in chromatin loop contact propensity are associated with differential gene regulation and expression

Project description:We quantitatively interrogate these relationships by comparing Hi-C and molecular phenotype data across cell types and haplotypes. While chromatin loops consistently form across different cell types, subtle quantitative differences in contact frequency are associated with larger changes in gene expression and H3K27ac. Across haplotypes, we find larger differences in contact frequency at imprinted and copy number variable loci. We find most changes in contact frequency are smaller across haplotypes than cell types; however, the proportional relationship between these changes and those in gene expression and regulation are consistent. This suggests that subtle changes in contact propensity have a biologically meaningful role in gene regulation and could be a mechanism by which regulatory genetic variants in loop anchors mediate effects on expression. The raw data files for these processed files can be obtained through dbGaP accession phs000924.

2019-01-24 | GSE125540 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data