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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 [ATAC-seq]

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

Project description:Highly coordinated changes in gene expression underlie T cell activation and exhaustion. However, the mechanisms by which such programs are regulated and how these may be targeted for therapeutic benefit remain poorly understood. Here, we comprehensively profile the genomic occupancy of mSWI/SNF chromatin remodeling complexes throughout acute and chronic T cell stimulation, finding that stepwise changes in localization over transcription factor binding sites direct site-specific chromatin accessibility and gene activation leading to distinct phenotypes. Notably, perturbation of mSWI/SNF complexes using genetic and clinically relevant chemical strategies enhances the persistence of T cells with attenuated exhaustion hallmarks and increased memory features in vitro and in vivo. Finally, pharmacologic mSWI/SNF inhibition improves CAR-T expansion and results in improved anti-tumor control in vivo. These findings reveal the central role of mSWI/SNF complexes in the coordination of T cell activation and exhaustion and nominate small-molecule-based strategies for the improvement of current immunotherapy protocols.

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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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Shifted assembly and function of mSWI/SNF family subcomplexes underlie targetable dependencies in endometriod carcinomas

Project description:The mammalian SWI/SNF (mSWI/SNF) family of chromatin remodelers govern cell type-specific chromatin accessibility and gene expression and assemble as three distinct complexes: canonical BAF (cBAF), Polybromo-associated BAF (PBAF), and non-canonical BAF (ncBAF). ARID1A and ARID1B are paralog subunits that specifically nucleate the assembly of cBAF complexes and are frequently dual deleted in highly aggressive differentiated endometrial carcinomas (DECs). Here, in cellular models and primary human tumors, we find that ARID1A/B-mediated cBAF loss results in increased ncBAF and PBAF biochemical abundance and function genome-wide to maintain the DEC oncogenic signature. Further, treatment of ARID1A/1B-mutant cell lines and PDX models in vivo with a clinical-grade SMARCA4/2 ATPase inhibitor, FHD-286, markedly attenuates cell proliferation and tumor growth, and synergizes with carboplatin-based chemotherapy. Taken together, these findings reveal the oncogenic contributions of shifted of mSWI/SNF family complex abundance and chromatin-level gene regulatory functions and suggest therapeutic utility of mSWI/SNF complex small molecule inhibitors in dedifferentiated endometrial carcinoma and other cBAF-disrupted cancer types.

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