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SWI/SNF directed epigenetic and transcriptional response during macrophage inflammatory activation.

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

ORGANISM(S): Mus musculus

PROVIDER: GSE242803 | GEO | 2024/06/05

REPOSITORIES: GEO

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SWI/SNF directed epigenetic and transcriptional response during macrophage inflammatory activation.

Project description:SWI/SNF directed epigenetic and transcriptional response during macrophage inflammatory activation.

| PRJNA1014761 | ENA

SWI/SNF localization during macrophage inflammatory response [ChIP-seq_SWISNF]

Project description:To understand how the SWI/SNF complex help establish appropriate epiegentic landscape during macrophage inflammatory response, we profiled the binding sites of BRG1 (all BAF), ARID1A (cBAF), BRD9 (ncBAF), and PHF10 (PBAF) for WT BMDMs with 0hr, 1hr, or 4hr LipidA stimulation. To assess the modes of action for cBAF inhibitor BRDK98, we also performed ARID1A ChIP for BRDK98-treated BDMDs after 0hr and 4hr of LipidA stimulation.

2024-06-05 | GSE242801 | GEO

Adenovirus E1A specifically blocks SWI/SNF-dependent transcriptional activation.

Project description:Expression of the adenovirus E1A243 oncoprotein in Saccharomyces cerevisiae produces a slow-growth phenotype with accumulation of cells in the G1 phase of the cell cycle. This effect is due to the N-terminal and CR1 domains of E1A243, which in rodent cells are involved in triggering cellular transformation and also in binding to the cellular transcriptional coactivator p300. A genetic screen was undertaken to identify genes required for the function of E1A243 in S. cerevisiae. This screen identified SNF12, a gene encoding the 73-kDa subunit of the SWI/SNF transcriptional regulatory complex. Mutation of genes encoding known members of the SWI/SNF complex also led to loss of E1A function, suggesting that the SWI/SNF complex is a target of E1A243. Moreover, expression of E1A in wild-type cells specifically blocked transcriptional activation of the INO1 and SUC2 genes, whose activation pathways are distinct but have a common requirement for the SWI/SNF complex. These data demonstrate a specific functional interaction between E1A and the SWI/SNF complex and suggest that a similar interaction takes place in rodent and human cells.

| S-EPMC231574 | biostudies-other

Epigenetic antagonism between polycomb and SWI/SNF complexes during oncogenic transformation.

Project description:Epigenetic alterations have been increasingly implicated in oncogenesis. Analysis of Drosophila mutants suggests that Polycomb and SWI/SNF complexes can serve antagonistic developmental roles. However, the relevance of this relationship to human disease is unclear. Here, we have investigated functional relationships between these epigenetic regulators in oncogenic transformation. Mechanistically, we show that loss of the SNF5 tumor suppressor leads to elevated expression of the Polycomb gene EZH2 and that Polycomb targets are broadly H3K27-trimethylated and repressed in SNF5-deficient fibroblasts and cancers. Further, we show antagonism between SNF5 and EZH2 in the regulation of stem cell-associated programs and that Snf5 loss activates those programs. Finally, using conditional mouse models, we show that inactivation of Ezh2 blocks tumor formation driven by Snf5 loss.

| S-EPMC2957473 | biostudies-literature

SWI/SNF localization during macrophage inflammatory response [ChIP-seq_SWISNF]

Project description:SWI/SNF localization during macrophage inflammatory response [ChIP-seq_SWISNF]

| PRJNA1014768 | ENA

A lncRNA-SWI/SNF complex crosstalk controls transcriptional activation at specific promoter regions.

Project description:LncRNAs have been shown to be direct players in chromatin regulation, but little is known about their role at active genomic loci. We investigate the role of lncRNAs in gene activation by profiling the RNA interactome of SMARCB1-containing SWI/SNF complexes in proliferating and senescent conditions. The isolation of SMARCB1-associated transcripts, together with chromatin profiling, shows prevalent association to active regions where SMARCB1 differentially binds locally transcribed RNAs. We identify SWINGN, a lncRNA interacting with SMARCB1 exclusively in proliferating conditions, exerting a pro-oncogenic role in some tumor types. SWINGN is transcribed from an enhancer and modulates the activation of GAS6 oncogene as part of a topologically organized region, as well as a larger network of pro-oncogenic genes by favoring SMARCB1 binding. Our results indicate that SWINGN influences the ability of the SWI/SNF complexes to drive epigenetic activation of specific promoters, suggesting a SWI/SNF-RNA cooperation to achieve optimal transcriptional activation.

| S-EPMC7028943 | biostudies-literature

Activator-dependent recruitment of SWI/SNF and INO80 during INO1 activation.

Project description:Transcriptional activation of yeast INO1 requires SWI/SNF and INO80 for nucleosome disruption at the promoter. However, the cooperative interplay among remodelers and their recruitment dynamics in activation have thus far been vague. Here, we showed, using chromatin immunoprecipitation, that both SWI/SNF and INO80 are present at the promoter and are restricted to the promoter, indicating that they directly participate in localized INO1 chromatin remodeling. Furthermore, both SWI/SNF and INO80 are absent at the INO1 promoter in ino2Delta cells, suggesting that these are activator-dependent remodelers. We have also found that the presence of INO80 is required for SWI/SNF recruitment, indicating that INO80 arrives first at the promoter followed by SWI/SNF. In light of these findings, we proposed a model which describes the order of events in INO1 activation.

| S-EPMC2536487 | biostudies-literature

Spn1 regulates the recruitment of Spt6 and the Swi/Snf complex during transcriptional activation by RNA polymerase II.

Project description:We investigated the timing of the recruitment of Spn1 and its partner, Spt6, to the CYC1 gene. Like TATA binding protein and RNA polymerase II (RNAPII), Spn1 is constitutively recruited to the CYC1 promoter, although levels of transcription from this gene, which is regulated postrecruitment of RNAPII, are low. In contrast, Spt6 appears only after growth in conditions in which the gene is highly transcribed. Spn1 recruitment is via interaction with RNAPII, since an spn1 mutant defective for interaction with RNAPII is not targeted to the promoter, and Spn1 is necessary for Spt6 recruitment. Through a targeted genetic screen, strong and specific antagonizing interactions between SPN1 and genes encoding Swi/Snf subunits were identified. Like Spt6, Swi/Snf appears at CYC1 only after activation of the gene. However, Spt6 significantly precedes Swi/Snf occupancy at the promoter. In the absence of Spn1 recruitment, Swi/Snf is constitutively found at the promoter. These observations support a model whereby Spn1 negatively regulates RNAPII transcriptional activity by inhibiting recruitment of Swi/Snf to the CYC1 promoter, and this inhibition is abrogated by the Spn1-Spt6 interaction. These findings link Spn1 functions to the transition from an inactive to an actively transcribing RNAPII complex at a postrecruitment-regulated promoter.

| S-EPMC2258746 | biostudies-literature

Effect of SWI/SNF pertubations on H3K27ac levels during macrophage inflammatory activation [ChIP-seq_Histone]

Project description:To understand how macrophage histone modifications respond to LipidA stimulation, we profiled H3K27ac binding for WT BMDMs with 0hr or 4hr LipidA stimulation. In addition, we also profiled H3k27ac levels for WT BMDMs treated with ACBI1, BRM014, BRDK98, or dBrd9 and for Arid1A-/- and Pbrm1-/- BMDMs after 4hr LipidA stimulation.

2024-06-05 | GSE242800 | GEO

Effect of SWI/SNF pertubations on chromatin accessibility during macrophage inflammatory activation [ATAC-seq]

Project description:To understand how macrophage chromatin respond to LipidA stimulation, we profiled accessibility for WT BMDMs with 0hr, 1hr, or 4hr LipidA stimulation. In addition, we also profiled accessibility for WT BMDMs treated with ACBI1, BRM014, BRDK98, or dBrd9 and for Arid1A-/- Pbrm1-/- BMDMs after 0hr, 1hr, or 4hr LipidA stimulation.

2024-06-05 | GSE242799 | GEO

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