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Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion [RNA-seq]

ABSTRACT: Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion [RNA-seq]

PROVIDER: PRJNA875107 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21354555.fastq.gz	Fastqsanger.gz
	SRR21354556.fastq.gz	Fastqsanger.gz
	SRR21354557.fastq.gz	Fastqsanger.gz
	SRR21354558.fastq.gz	Fastqsanger.gz
	SRR21354559_1.fastq.gz	Fastqsanger.gz

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Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion [RNA-seq]

Project description:This study comprehensively profiles the mSWI/SNF complexes throughout acute and chronic T cell stimulation, with and without small molecular inhibitors and degraders. Specifically, we find pan SWI/SNF and complex specific roles in both activation and exhaustion.

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Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion [Cut&Tag]

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Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion

Project description:Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion

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Project description:Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion [ATAC-seq]

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Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion

Project description:This SuperSeries is composed of the SubSeries listed below.

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Structural and functional properties of mSWI/SNF chromatin remodeling complexes revealed through single-cell perturbation and genomic profiling

Project description:Mammalian SWI/SNF (mSWI/SNF or BAF) chromatin remodeling complexes play critical roles in regulating DNA accessibility and gene expression and are comprised of three final-form assemblies, cBAF, PBAF, and ncBAF, which exhibit distinct modular organization, chromatin targeting, and roles in disease. However, the contributions of each subcomplex and their constituent subunits to gene expression remain incompletely defined. Here, we performed a large-scale CRISPR-Cas9 knockout screen targeting mSWI/SNF subunits individually and in selected combinations, followed by single-cell RNA-sequencing (Perturb-seq) and SHARE-Seq. We uncover complex- and module-specific contributions across cell regulatory pathways, define paralog subunit relationships, and identify shifted functions upon perturbations. Finally, we superimpose single-cell perturbation signatures over bulk primary human tumor gene expression profiles, defining unique subunit-specific signatures and identifying tumor features that mirror BAF loss-of-function. Taken together, these data highlight the utility of large-scale single-cell genomics to uncover gene expression and chromatin accessibility signatures in human disease states.

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Project description:Recent exon sequencing studies of human tumors have revealed that subunits of mSWI/SNF or BAF complexes are mutated in more than 20% of human malignancies, yet the mechanisms involved in tumor suppression is unclear. BAF chromatin remodeling complexes are polymorphic assemblies that use energy provided by ATP hydrolysis to regulate transcription through the control of chromatin structure and the placement of Polycomb (PcG) across the genome. Several proteins dedicated to this large multi-subunit complex, including SMARCA4 (BRG1) and BAF250A (ARID1A), are mutated at frequencies similar to that of many recognized tumor suppressors. In particular, the core ATPase BRG1 is mutated in 5-10% of childhood medulloblastoma (MB) and greater than 15% of Burkitt's Lymphoma (BL). Here we find a novel function of BAF complexes in decatenating newly replicated sister chromatids, which is necessary for proper chromosome segregation during mitosis. We find that deletion of Brg1, as well as the expression of Brg1 point mutants identified in human tumors leads to anaphase bridge formation (sister chromatids linked by catenated strands of DNA), and a G2/M phase block characteristic of the decatenation checkpoint. Endogenous BAF complexes directly interact with endogenous TopoIIα through BAF250a and are required for TopoIIα binding to about 12,000 sites over the genome. Our results indicate that TopoIIα’s chromatin binding is dependent on the ATPase activity of Brg1, which is compromised in oncogenic Brg1 mutants. These studies indicate that the ability of TopoIIα to prevent DNA entanglement at mitosis requires BAF complexes and suggest that this activity contributes to the role of BAF subunits as tumor suppressors. Examination of sites of TopoIIa activity in WT and Brg1-/- ES cells as defined by TopoIIa-DNA covalent adducts formed in the presence of etoposide

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