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HMGA1 causes a global shift in chromatin architecture linked to transcriptional changes

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE245808 | GEO | 2024/07/08

REPOSITORIES: GEO

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HMGA1 causes a global shift in chromatin architecture linked to transcriptional changes [scRNA-Seq]

Project description:High Mobility Group A1 (HMGA1) is an architectural chromatin-binding protein that regulates gene expression in various biological contexts, including differentiation and cancer. While previous studies show that HMGA1 acts by binding specific gene promoters or by contributing to the enhanceosome, its global effect on transcription remains unclear. HMGA1 is also critical for the formation of senescence-associated heterochromatic foci (SAHF) in oncogene-induced senescence (OIS), a stable form of cell cycle arrest with a pro-inflammatory phenotype. This link between the two roles of HMGA1, gene regulation and chromatin organisation, has not been fully explained. Here, we used graph theory and data integration from high-throughput assays to investigate how HMGA1 binding impacts the chromatin interactions network. Our results demonstrate that HMGA1 profoundly remodels the global chromatin network during OIS and contributes to stronger compartmentalization. This remodelling goes beyond SAHF, leading to substantial gene repositioning and differential gene expression, highlighting a novel role for HMGA1 in altering chromatin environments. The HMGA1 effects of gene expression go beyond senescence and appear to be relevant in other contexts, such as lung cancer.

2024-07-08 | GSE245807 | GEO

HMGA1 causes a global shift in chromatin architecture linked to transcriptional changes [Hi-C]

2024-07-08 | GSE245804 | GEO

HMGA1 causes a global shift in chromatin architecture linked to transcriptional changes [ChIP-Seq]

2024-07-08 | GSE245802 | GEO

HMGA1 causes a global shift in chromatin architecture linked to transcriptional changes [RNA-Seq]

2024-07-08 | GSE245801 | GEO

HMGA1 causes a global shift in chromatin architecture linked to transcriptional changes

Project description:HMGA1 causes a global shift in chromatin architecture linked to transcriptional changes

| PRJNA1029997 | ENA

HMGA1 causes a global shift in chromatin architecture linked to transcriptional changes [ChIP-Seq]

Project description:HMGA1 causes a global shift in chromatin architecture linked to transcriptional changes [ChIP-Seq]

| PRJNA1029992 | ENA

HMGA1 causes a global shift in chromatin architecture linked to transcriptional changes [RNA-Seq]

Project description:HMGA1 causes a global shift in chromatin architecture linked to transcriptional changes [RNA-Seq]

| PRJNA1029989 | ENA

HMGA1 causes a global shift in chromatin architecture linked to transcriptional changes [scRNA-Seq]

Project description:HMGA1 causes a global shift in chromatin architecture linked to transcriptional changes [scRNA-Seq]

| PRJNA1030004 | ENA

HMGA1 causes a global shift in chromatin architecture linked to transcriptional changes [Hi-C]

Project description:HMGA1 causes a global shift in chromatin architecture linked to transcriptional changes [Hi-C]

| PRJNA1030006 | ENA

Hsf1 and Hsp90 orchestrate temperature-dependent global transcriptional remodelling and chromatin architecture in Candida albicans.

Project description:Fever is a universal response to infection, and opportunistic pathogens such as Candida albicans have evolved complex circuitry to sense and respond to heat. Here we harness RNA-seq and ChIP-seq to discover that the heat shock transcription factor, Hsf1, binds distinct motifs in nucleosome-depleted promoter regions to regulate heat shock genes and genes involved in virulence in C. albicans. Consequently, heat shock increases C. albicans host cell adhesion, damage and virulence. Hsf1 activation depends upon the molecular chaperone Hsp90 under basal and heat shock conditions, but the effects are opposite and in part controlled at the level of Hsf1 expression and DNA binding. Finally, we demonstrate that Hsp90 regulates global transcription programs by modulating nucleosome levels at promoters of stress-responsive genes. Thus, we describe a mechanism by which C. albicans responds to temperature via Hsf1 and Hsp90 to orchestrate gene expression and chromatin architecture, thereby enabling thermal adaptation and virulence.

| S-EPMC4894976 | biostudies-literature

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