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Epigenetic dependencies of interferon gamma-induced gene expression [ChIP-Seq]

ABSTRACT: Epigenetic dependencies of interferon gamma-induced gene expression [ChIP-Seq]

PROVIDER: PRJNA833410 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18972429.fastq.gz	Fastqsanger.gz
	SRR18972430.fastq.gz	Fastqsanger.gz
	SRR18972431.fastq.gz	Fastqsanger.gz
	SRR18972432.fastq.gz	Fastqsanger.gz
	SRR18972433.fastq.gz	Fastqsanger.gz

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Project description:Interferon gamma (IFNy) is a pro-inflammatory cytokine that directly activates the JAK/STAT pathway. However, the temporal dynamics of chromatin remodeling and transcriptional activation initiated by IFN have not been systematically profiled in an unbiased manner. Herein, we integrated transcriptomic and epigenomic profiling to characterize the acute epigenetic changes induced by IFNy stimulation in a murine breast cancer model. We identified de novo activation of cis-regulatory elements bound by Irf1 that were characterized by increased chromatin accessibility, differential usage of pro-inflammatory enhancers, and downstream recruitment of BET proteins and RNA polymerase II. To functionally validate this hierarchical model of IFNy-driven transcription, we applied selective antagonists of histone acetyltransferases P300/CBP or acetyl-lysine readers of the BET family. This highlighted that histone acetylation is an antecedent event in IFNy-driven transcription, whereby targeting of P300/CBP but not BET inhibition, could curtail the epigenetic remodeling induced by IFNy through suppression of Irf1 transactivation. These data highlight the utility for epigenetic therapies to reprogram pro-inflammatory gene expression, which may have therapeutic implications for anti-tumor immunity and inflammatory diseases.

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