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Chromatin accessibility profiling in STAG2 mutant K562 cells

ABSTRACT: Chromatin accessibility profiling in STAG2 mutant K562 cells

PROVIDER: PRJNA543744 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9090310.fastq.gz	Fastqsanger.gz
	SRR9090302.fastq.gz	Fastqsanger.gz
	SRR9090303.fastq.gz	Fastqsanger.gz
	SRR9090304.fastq.gz	Fastqsanger.gz
	SRR9090305.fastq.gz	Fastqsanger.gz

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Chromatin accessibility and expression profiling in STAG2 mutant K562 cells

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Chromatin accessibility profiling in STAG2 mutant K562 cells

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Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation [RNA_3populations_LSK_GMP_CFUE]

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Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation [ChIP_LinNeg_Stag1Stag2CTCF]

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Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation [ATAC_LinNegBM]

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Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation [RNA_LinNegBM]

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STAG2 mutations and 3D genome organization, chromatin loops, and polycomb signaling in glioblastoma multiforme

Project description:Inactivating mutations of genes encoding the cohesin complex are common in a wide range of human cancers. STAG2 is the most commonly mutated subunit. Here we report the impact of stable correction of endogenous, naturally occurring STAG2 mutations on gene expression, 3D genome organization, chromatin loops, and Polycomb signaling in glioblastoma multiforme. Correction of mutant STAG2 significantly altered the expression of ~10% of all expressed genes. The genes most highly regulated by STAG2 (e.g. FGF7, c-KIT, MAGE tumor antigens) were virtually all upregulated in STAG2-mutant cells. Hi-C revealed that ~3% of A/B compartments switched after STAG2 correction, and confirmed prior findings that STAG2 is dispensable for maintenance of Topologically Associating Domains (TADs). The size and strength of thousands of chromatin loops were altered by STAG2 correction, a subset of which controlled the expression of adjacent genes. Loops specific to STAG2-mutant cells and tumors were very large, supporting prior findings that STAG1-containing cohesin complexes have greater loop extrusion processivity than STAG2-containing cohesin complexes, and suggesting that long loops may be a generalizable feature of STAG2-mutant cancers. Finally, STAG2-regulated chromatin loops were enriched for the H3K27me3 Polycomb epigenetic mark, revealing that inactivation of STAG2 can activate Polycomb signaling in GBM. Together these findings illuminate the landscape of STAG2-regulated genes, A/B compartments, chromatin loops, and pathways in GBM, providing important clues into the still mysterious mechanism of STAG2 tumor suppression in human cancer.

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