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Study of MED1 acetylation in ER positive breast cancer cells [ChIP-seq]

ABSTRACT: Chromatin occupancy of MED1 and other Mediator components, as well as Pol II, were studied in MCF7 cells. MED1 acetylation affects chromatin occupancy of its related factors, which was analyzed with CUT&RUN-seq, ChIP-seq and sequential ChIP-seq assay (by pan-acetyl-lysine antibody) with MED1 KR mutant (HA tag) where acetylation residues were replaced. Combined with RNA seq analysis for gene expression in MCF7 cells with MED1 KO and KR/KQ MED1 ectopic expression, the role of MED1 acetylation in gene transcription control was investigated.

ORGANISM(S): Homo sapiens

PROVIDER: GSE245868 | GEO | 2025/08/01

REPOSITORIES: GEO

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Study of MED1 acetylation in ER positive breast cancer cells [CUT&Run]

Project description:Chromatin occupancy of MED1 and other Mediator components, as well as Pol II, were studied in MCF7 cells. MED1 acetylation affects chromatin occupancy of its related factors, which was analyzed with CUT&RUN-seq, ChIP-seq and sequential ChIP-seq assay (by pan-acetyl-lysine antibody) with MED1 KR mutant (HA tag) where acetylation residues were replaced. Combined with RNA seq analysis for gene expression in MCF7 cells with MED1 KO and KR/KQ MED1 ectopic expression, the role of MED1 acetylation in gene transcription control was investigated.

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Disruption of cardiac Med1 inhibits RNA polymerase-II promoter occupancy and induces chromatin remodeling

Project description:The Mediator co-activator complex directs gene specific expression by binding distal enhancer-bound transcription factors through its Med1 subunit while bridging to RNA Polymerase-II (Pol-II) at gene promoters. In addition, Mediator scaffolds epigenetic modifying enzymes that determine local DNA accessibility. We previously found that deletion of Med1 in cardiomyocytes deregulates more than 5000 genes and promotes acute heart failure and hypothesize Med1 deficiency disrupts enhancer-promoter coupling. Using ChIP-seq, we find Pol-II pausing index is increased in Med1 knockout versus floxed control hearts primarily from decreased Pol-II occupancy at the majority of transcriptional start sites. Med1-dependent gene expression correlates strongly with histone H3 K27 acetylation while H3 K27 tri-methylated levels are increased and inversely correlate with absolute expression levels. Furthermore, Med1 deletion leads to dynamic changes in acetyl-K27 associated super-enhancer regions and their enriched transcription factor binding motifs that are consistent with altered gene expression. Our findings suggest that Med1 is important in establishing enhancer-promoter coupling in the heart by facilitating the recruitment of Pol-II to gene promoters, determining chromatin accessibility within genes and enhancer regions and altering transcription factor binding motifs that are likely important in directing gene-specific expression.

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