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The Mediator Kinase Complex Cooperates with Swi/Snf to Regulate Lineage-Resolved Enhancers and Differentiation

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

ORGANISM(S): Mus musculus

PROVIDER: GSE191124 | GEO | 2022/10/19

REPOSITORIES: GEO

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The Mediator Kinase Complex Cooperates with Swi/Snf to Regulate Lineage-Resolved Enhancers and Differentiation [RNA-Seq]

Project description:To identify novel functions of Mediator kinases CDK8 and CDK19 in the intestinal epithelium, we generated novel genetic mouse model enabling the individual and compound deletion of CDK8 and CDK19. RNA-sequencing was performed on primary intestinal epithelial cells and murine small intestinal organoids at different time points after CDK8/19 deletion.

2022-10-19 | GSE191123 | GEO

The Mediator Kinase Complex Cooperates with Swi/Snf to Regulate Lineage-Resolved Enhancers and Differentiation [ChIP-Seq]

Project description:Depletion of CDK8 and its paralogue CDK19 in intestinal organoids resulted in the downregulation of genes associated with intestinal secretory cells. To determine the consequence of loss of CDK8/19 in re-defining enhancers we performed ChIP sequencing for MED1, MED12, H3K27Ac and ARID1A. We identified that loss of MED1 and MED12 at super enhancers regulating key intestinal transcription factors and loss of ARID1A binding across intestinal (super-)enhancers.

2022-10-19 | GSE191121 | GEO

The Mediator Kinase Complex Cooperates with Swi/Snf to Regulate Lineage-Resolved Enhancers and Differentiation

Project description:The Mediator Kinase Complex Cooperates with Swi/Snf to Regulate Lineage-Resolved Enhancers and Differentiation

| PRJNA789825 | ENA

The Mediator Kinase Complex Cooperates with Swi/Snf to Regulate Lineage-Resolved Enhancers and Differentiation [RNA-Seq]

Project description:The Mediator Kinase Complex Cooperates with Swi/Snf to Regulate Lineage-Resolved Enhancers and Differentiation [RNA-Seq]

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The Mediator Kinase Complex Cooperates with Swi/Snf to Regulate Lineage-Resolved Enhancers and Differentiation [ChIP-Seq]

Project description:The Mediator Kinase Complex Cooperates with Swi/Snf to Regulate Lineage-Resolved Enhancers and Differentiation [ChIP-Seq]

| PRJNA789836 | ENA

The SWI/SNF chromatin remodelling complex is required for maintenance of lineage specific enhancers.

Project description:Genes encoding subunits of SWI/SNF (BAF) chromatin remodelling complexes are collectively altered in over 20% of human malignancies, but the mechanisms by which these complexes alter chromatin to modulate transcription and cell fate are poorly understood. Utilizing mouse embryonic fibroblast and cancer cell line models, here we show via ChIP-seq and biochemical assays that SWI/SNF complexes are preferentially targeted to distal lineage specific enhancers and interact with p300 to modulate histone H3 lysine 27 acetylation. We identify a greater requirement for SWI/SNF at typical enhancers than at most super-enhancers and at enhancers in untranscribed regions than in transcribed regions. Our data further demonstrate that SWI/SNF-dependent distal enhancers are essential for controlling expression of genes linked to developmental processes. Our findings thus establish SWI/SNF complexes as regulators of the enhancer landscape and provide insight into the roles of SWI/SNF in cellular fate control.

| S-EPMC5343482 | biostudies-literature

The histone reader PHF7 cooperates with the SWI/SNF complex at cardiac super enhancers to promote direct reprogramming.

Project description:Direct cardiac reprogramming of fibroblasts to cardiomyocytes presents an attractive therapeutic strategy to restore cardiac function following injury. Cardiac reprogramming was initially achieved through overexpression of the transcription factors Gata4, Mef2c and Tbx5; later, Hand2 and Akt1 were found to further enhance this process1-5. Yet, staunch epigenetic barriers severely limit the ability of these cocktails to reprogramme adult fibroblasts6,7. We undertook a screen of mammalian gene regulatory factors to discover novel regulators of cardiac reprogramming in adult fibroblasts and identified the histone reader PHF7 as the most potent activating factor8. Mechanistically, PHF7 localizes to cardiac super enhancers in fibroblasts, and through cooperation with the SWI/SNF complex, it increases chromatin accessibility and transcription factor binding at these sites. Furthermore, PHF7 recruits cardiac transcription factors to activate a positive transcriptional autoregulatory circuit in reprogramming. Importantly, PHF7 achieves efficient reprogramming in the absence of Gata4. Here, we highlight the underexplored necessity of cardiac epigenetic readers, such as PHF7, in harnessing chromatin remodelling and transcriptional complexes to overcome critical barriers to direct cardiac reprogramming.

| S-EPMC8243412 | biostudies-literature

Mutant p53 cooperates with the SWI/SNF chromatin remodeling complex to regulate VEGFR2 in breast cancer cells.

Project description:Mutant p53 impacts the expression of numerous genes at the level of transcription to mediate oncogenesis. We identified vascular endothelial growth factor receptor 2 (VEGFR2), the primary functional VEGF receptor that mediates endothelial cell vascularization, as a mutant p53 transcriptional target in multiple breast cancer cell lines. Up-regulation of VEGFR2 mediates the role of mutant p53 in increasing cellular growth in two-dimensional (2D) and three-dimensional (3D) culture conditions. Mutant p53 binds near the VEGFR2 promoter transcriptional start site and plays a role in maintaining an open conformation at that location. Relatedly, mutant p53 interacts with the SWI/SNF complex, which is required for remodeling the VEGFR2 promoter. By both querying individual genes regulated by mutant p53 and performing RNA sequencing, the results indicate that >40% of all mutant p53-regulated gene expression is mediated by SWI/SNF. We surmise that mutant p53 impacts transcription of VEGFR2 as well as myriad other genes by promoter remodeling through interaction with and likely regulation of the SWI/SNF chromatin remodeling complex. Therefore, not only might mutant p53-expressing tumors be susceptible to anti VEGF therapies, impacting SWI/SNF tumor suppressor function in mutant p53 tumors may also have therapeutic potential.

| S-EPMC4495400 | biostudies-literature

The Hippo transducer TAZ interacts with the SWI/SNF complex to regulate breast epithelial lineage commitment.

Project description:Lineage-committed cells of many tissues exhibit substantial plasticity in contexts such as wound healing and tumorigenesis, but the regulation of this process is not well understood. We identified the Hippo transducer WWTR1/TAZ in a screen of transcription factors that are able to prompt lineage switching of mammary epithelial cells. Forced expression of TAZ in luminal cells induces them to adopt basal characteristics, and depletion of TAZ in basal and/or myoepithelial cells leads to luminal differentiation. In human and mouse tissues, TAZ is active only in basal cells and is critical for basal cell maintenance during homeostasis. Accordingly, loss of TAZ affects mammary gland development, leading to an imbalance of luminal and basal populations as well as branching defects. Mechanistically, TAZ interacts with components of the SWI/SNF complex to modulate lineage-specific gene expression. Collectively, these findings uncover a new role for Hippo signaling in the determination of lineage identity through recruitment of chromatin-remodeling complexes.

| S-EPMC4011189 | biostudies-literature

Pioneer-like factor GAF cooperates with PBAP (SWI/SNF) and NURF (ISWI) to regulate transcription.

Project description:Transcriptionally silent genes must be activated throughout development. This requires nucleosomes be removed from promoters and enhancers to allow transcription factor (TF) binding and recruitment of coactivators and RNA polymerase II (Pol II). Specialized pioneer TFs bind nucleosome-wrapped DNA to perform this chromatin opening by mechanisms that remain incompletely understood. Here, we show that GAGA factor (GAF), a Drosophila pioneer-like factor, functions with both SWI/SNF and ISWI family chromatin remodelers to allow recruitment of Pol II and entry to a promoter-proximal paused state, and also to promote Pol II's transition to productive elongation. We found that GAF interacts with PBAP (SWI/SNF) to open chromatin and allow Pol II to be recruited. Importantly, this activity is not dependent on NURF as previously proposed; however, GAF also synergizes with NURF downstream from this process to ensure efficient Pol II pause release and transition to productive elongation, apparently through its role in precisely positioning the +1 nucleosome. These results demonstrate how a single sequence-specific pioneer TF can synergize with remodelers to activate sets of genes. Furthermore, this behavior of remodelers is consistent with findings in yeast and mice, and likely represents general, conserved mechanisms found throughout eukarya.

| S-EPMC7778264 | biostudies-literature

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