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Effect of BAF disruption on chromatin accessibility in activated CD8+ T cells [ATAC-seq]

ABSTRACT: Effect of BAF disruption on chromatin accessibility in activated CD8+ T cells [ATAC-seq]

PROVIDER: PRJNA983073 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23958775_1.fastq.gz	Fastqsanger.gz
	SRR23958775_2.fastq.gz	Fastqsanger.gz
	SRR23958776_1.fastq.gz	Fastqsanger.gz
	SRR23958776_2.fastq.gz	Fastqsanger.gz
	SRR23958777_1.fastq.gz	Fastqsanger.gz

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Effect of BAF disruption on T-bet binding in activated CD8+ T cells [ChIP-seq]

Project description:Effect of BAF disruption on T-bet binding in activated CD8+ T cells [ChIP-seq]

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Acute BAF perturbation causes immediate changes in chromatin accessibility

Project description:Loss-of-function mutations in genes coding for subunits of the large, multifarious BRG1/BRM associated factor (BAF) chromatin remodeling complexes are frequently causative for cancer or developmental diseases1-5. Cells lacking the most frequently mutated subunits like the ATPase SMARCA4 typically exhibit drastic chromatin accessibility changes, especially of important regulatory regions6-12. However, so far it remains unknown how these changes are established over time, and whether they are causative for intra-complex synthetic lethalities abrogating the formation (SMARCC1-SMARCC2)8,13,14 or activity (SMARCA4-SMARCA2)15-17 of BAF complexes. Here, we utilize the dTAG system18 to induce acute degradation of BAF subunits in wild-type and BAF mutant backgrounds and analyze the resulting chromatin accessibility changes with high kinetic resolution. We observe that chromatin alterations are established faster than the duration of one cell cycle and that maintaining genome accessibility requires constant ATP-dependent remodeling. Completely abolishing BAF complex function by acute degradation of a synthetic lethal subunit in a paralog-deficient background results in a near-complete loss of chromatin accessibility at BAF-controlled sites, especially at super-enhancers, providing a mechanism for intra-complex synthetic lethalities.

2020-12-23 | PXD018381 | Pride

Effect of BAF disruption on chromatin accessibility in activated CD8+ T cells [ATAC-seq]

Project description:To investigate the role of cBAF in regulation of Tbet binding, polyclonal naive CD8 T cells were stimulated for 48h with anti-CD3, CD28, and hIL-2. Cells were then treated with DMSO, ACBI1, or BRM014 for 6 hours, and treated with recombinant mouse IL-12 for the last two hours of inhibitor treatment. Chromatin accessibility profiling was performed via ATAC-seq.

2023-06-13 | GSE228193 | GEO

Chromatin accessibility changes after BAF complex disruption in neuroblastoma cells by ATAC-Seq

Project description:In order to study the genomic regions undergoing chromatin accessibility changes when BAF chromatin remodelling complex is inhibited, ATAC-Seq of SK-N-BE(2) neuroblastoma cells was performed after silencing of BAF structural subunits ARID1A and ARID1B.

2022-11-01 | GSE202306 | GEO

Chromatin accessibility changes after BAF complex disruption in neuroblastoma cells by ATAC-Seq

Project description:Chromatin accessibility changes after BAF complex disruption in neuroblastoma cells by ATAC-Seq

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Acute BAF perturbation causes immediate changes in chromatin accessibility

Project description:Loss-of-function mutations in genes coding for subunits of the large, multifarious BRG1/BRM associated factor (BAF) chromatin remodeling complexes are frequently causative for cancer or developmental diseases. Cells lacking the most frequently mutated subunits, like the ATPase SMARCA4, typically exhibit drastic chromatin accessibility changes, especially of important regulatory regions. However, so far it remains unknown how these changes are established over time, and whether they are causative for intra-complex synthetic lethalities abrogating the formation or activity of BAF complexes. Here, we utilize the dTAG system to induce acute degradation of BAF subunits in wildtype and BAF mutant backgrounds and analyze the resulting chromatin accessibility changes with high kinetic resolution. We observe that chromatin alterations are established faster than the duration of one cell cycle and that maintaining genome accessibility requires constant ATP-dependent remodeling. Completely abolishing BAF complex function by acute degradation of a synthetic lethal subunit in a paralog-deficient background results in a near-complete loss of chromatin accessibility at BAF-controlled sites, especially at super-enhancers, providing a mechanism for intra-complex synthetic lethalities.

2020-12-22 | GSE148175 | GEO

BAF controls genome accessibility

Project description:Somatic differentiation requires induction of lineage specific genes to fulfill specialized tissue functions yet the genomic control of this process is incompletely understood. Using the epidermis as a model, we show here that the BAF chromatin remodeling complex is essential to maintain a subset of open chromatin regions, which are strikingly enriched for the DNA binding motif of the stratified epithelial lineage-determining transcription factor p63 (p=1X10-1786). These p63 sites are intrinsically inaccessible. BAF is required to displace nucleosomes ~40 base pairs away from p63 motifs to enable p63 binding, to maintain active histone marks, and to recruit RNA polymerase II to promote gene expression. In this process, p63 was itself also essential for full BAF recruitment to p63 binding sites. Intrinsically, p63 binding sequences favor nucleosome occupancy. Our data therefore suggest a model where a lineage-specific transcription factor cooperates with the BAF complex to establish genome accessibility and engage tissue-specific gene expression.

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Dynamic BAF chromatin remodeling complex subunit inclusion promotes temporally distinct gene expression programs in cardiogenesis

Project description:Chromatin remodeling complexes instruct cellular differentiation and lineage specific transcription. The BRG1/BRM associated factor (BAF) complexes are important for several aspects of differentiation. We show that the catalytic subunit Brg1 has a specific role in cardiac precursors (CPs) to initiate cardiac gene expression programs and repress non-cardiac expression. Using immunoprecipitation immunopurification with mass spectrometry we determined the dynamic composition of BAF complexes during mammalian cardiac differentiation, identifying several cell-type specific subunits. We focused on the CP- and cardiomyocytes (CM)-enriched subunits BAF60c (SMARCD3) and BAF170 (SMARCC2). Baf60c and Baf170 co-regulate gene expression with Brg1 in CPs, and in CMs their loss results in broadly deregulated cardiac gene expression. BRG1, BAF60, and BAF170 modulate chromatin accessibility, to either promote accessibility at activated genes, while closing up chromatin at repressed genes. BAF60c and BAF170 are required for proper BAF complex composition, and BAF170 loss leads to retention of BRG1 at CP-specific enhancers. Thus, dynamic interdependent BAF complex subunit assembly modulates chromatin states and thereby participates in directing temporal gene expression programs in cardiogenesis.

2019-11-13 | PXD012721 | Pride

Spliceosomal disruption of the non-canonical BAF complex in cancer

Project description:Spliceosomal disruption of the non-canonical BAF complex in cancer

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Acute BAF perturbation causes immediate changes in chromatin accessibility

Project description:Acute BAF perturbation causes immediate changes in chromatin accessibility

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