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A homeostatic Arid1a-dependent permissive chromatin state licenses hepatocyte responsiveness to liver injury-associated YAP signaling

ABSTRACT: A homeostatic Arid1a-dependent permissive chromatin state licenses hepatocyte responsiveness to liver injury-associated YAP signaling

PROVIDER: PRJNA437235 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6813700_1.fastq.gz	Fastqsanger.gz
	SRR6813700_2.fastq.gz	Fastqsanger.gz
	SRR6813710_1.fastq.gz	Fastqsanger.gz
	SRR6813710_2.fastq.gz	Fastqsanger.gz
	SRR6813701_1.fastq.gz	Fastqsanger.gz

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A homeostatic Arid1a-dependent permissive chromatin state licenses hepatocyte responsiveness to liver injury-associated YAP signaling (ChIP-seq)

Project description:A homeostatic Arid1a-dependent permissive chromatin state licenses hepatocyte responsiveness to liver injury-associated YAP signaling (ChIP-seq)

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A homeostatic Arid1a-dependent permissive chromatin state licenses hepatocyte responsiveness to liver injury-associated YAP signaling (ATAC-seq)

Project description:A homeostatic Arid1a-dependent permissive chromatin state licenses hepatocyte responsiveness to liver injury-associated YAP signaling (ATAC-seq)

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A homeostatic Arid1a-dependent permissive chromatin state licenses hepatocyte responsiveness to liver injury-associated YAP signaling (RNA-seq)

Project description:A homeostatic Arid1a-dependent permissive chromatin state licenses hepatocyte responsiveness to liver injury-associated YAP signaling (RNA-seq)

| PRJNA437240 | ENA

A homeostatic Arid1a-dependent permissive chromatin state licenses hepatocyte responsiveness to liver injury-associated YAP signaling (ChIP-seq)

Project description:Following injury, differentiated epithelial cells can serve as a stem cell-independent source for tissue regeneration by undergoing reprogramming into other cell types. The intrinsic molecular basis underlying plasticity of differentiated cells remains largely unaddressed. Here we show that Arid1a, a key component of the SWI/SNF chromatin remodeling complex, controls liver regeneration and gene expression associated with emergence of injury-induced progenitor-like cells (LPLCs). Hepatocyte-specific Arid1a ablation reduces LPLC gene expression in several models of periportal liver injury and impairs liver regeneration, leading to organ dysfunction. Arid1a establishes a permissive chromatin state at LPLC-enriched genes during homeostasis, suggesting it endows hepatocytes with competence to respond to injury-induced signals. Consistently, Arid1a facilitates binding of YAP, a critical regeneration signaling pathway, to LPLC-enriched genes, and Arid1a deletion prevents their YAP-associated induction following injury. Together, these findings provide a framework for studying the contributions of injury-induced LPLCs to periportal liver regeneration.

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A homeostatic Arid1a-dependent permissive chromatin state licenses hepatocyte responsiveness to liver injury-associated YAP signaling (RNA-seq)

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A homeostatic Arid1a-dependent permissive chromatin state licenses hepatocyte responsiveness to liver injury-associated YAP signaling (ATAC-seq)

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A homeostatic Arid1a-dependent permissive chromatin state licenses hepatocyte responsiveness to liver injury-associated YAP signaling

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

2019-07-07 | GSE111502 | GEO

RNA-seq in ARID1A WT, KO OVCA429 Cells after IFNγ treatment

Project description:Whether cancer driver mutation(s) directly drives cancer immune phenotype and immune tolerance remains a standing question. ARID1A is a core member of the polymorphic BAF chromatin remodeling complex. ARID1A mutations frequently occur in human cancers and drive cancer development. Here, we studied the molecular, cellular, and clinical impact of ARID1A gene status on cancer immunity. We demonstrate that ARID1A mutations, limited expression, and deficiency impair interferon(IFN)-responsive gene chromatin accessibility and expression, resulting in anemic T cell tumor infiltration, weakened tumor immunity, and shortened host survival in many human cancer histologies as well as in murine cancer models, and are negatively associated with immunotherapy response. Mechanistically, ARID1A interacts with EZH2 via its carboxyl terminal and antagonizes EZH2-mediated IFN responsiveness. Thus, the interaction between ARID1A and EZH2 defines cancer IFN-responsiveness and immune evasion. Our work indicates that cancer epigenetic driver mutations can shape cancer immune phenotype and immunotherapy.

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2020-05-06 | GSE131915 | GEO