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EZH2 inhibition with GSK343 reduces H3K27me3 deposition at various repetitive elements in splenic B cells [ChIP-Seq]

ABSTRACT: EZH2 inhibition with GSK343 reduces H3K27me3 deposition at various repetitive elements in splenic B cells [ChIP-Seq]

PROVIDER: PRJNA813876 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25406354_1.fastq.gz	Fastqsanger.gz
	SRR25406354_2.fastq.gz	Fastqsanger.gz
	SRR25406355_1.fastq.gz	Fastqsanger.gz
	SRR25406355_2.fastq.gz	Fastqsanger.gz
	SRR25406356_1.fastq.gz	Fastqsanger.gz

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EZH2 inhibition with GSK343 reduces H3K27me3 deposition at various repetitive elements in splenic B cells [ChIP-Seq]

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Project description:EZH2 is a histone methyltransferase that deposits H3K27me2/3 in heterochromatin and it is misregulated in tumorigenesis. Inhibition of heterochromatin can induce viral mimicry in cancer cells, where upregulated repetitive elements are detected by cytosolic pattern recognition receptors (PRRs) to activate inflammatory signaling. Here we demonstrate that EZH2 inhibitors stimulate inflammation and immune self-recognition of resting splenic B cells. We generated a PRR loss-of-function mouse model called RIC with mutations in Rigi, Ifih1 (MDA5), and Cgas. In both WT and RIC mutant B cells, EZH2 inhibition caused loss of H3K27me3 at repetitive elements and upregulated their expression. However, expression of inflammatory chemokines in B cells was interrupted by the RIC mutations. Furthermore, recruitment of cytotoxic T cells and neutrophils in response to EZH2 inhibition was blocked in RIC mutants preserving viability of B cells. This study demonstrates a pharmacologically induced mechanism of inflammation that causes self-recognition and B cell death.

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Project description:Our previous study has found that GSK343 is a potent autophagy inducer. To further investigate the underlying mechanisms, microarray analysis was performed.

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PolyA RNA-seq from retinoic acid-differentiated iPSCs treated with GSK343, 5-aza, or Combo (GSK343 & 5-aza)

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Cytosolic PRRs are required to upregulate interferon gene expression upon EZH2 inhibition with GSK343 in B16-F10 melanoma cells [RNA-seq]

Project description:EZH2 is a histone methyltransferase that deposits the repressive histone H3 lysine 27 trimethylation (H3K27me3). This mark has been reported to silence expression of various repetitive elements in the genome. We sought to identify the effect of EZH2 inhibition on coding and non-coding, repetitive RNA expression. We generated a novel mutant mouse line whose ability to detect induced repeat element expression has been abrogated. We report that the mutant splenic B cells fail to upregulate inflammatory gene expression upon EZH2 inhibition, despite comparable upregulation of various repetitive elements with WT. Unlike WT splenic B cells that do not upregulate interferon gene expression upon EZH2 inhibition, B16-F10 melanoma cells activate their expression under the same inhibitor treatment. Cytosolic pattern recognition receptors, RIG-I and Cgas, are required for such response as their deletion abrogates this pathway.

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