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Transient upregulation of IRF1 during the exit from naive pluripotency confers viral protection

ABSTRACT: IRF1 in exit from naive pluripotency

PROVIDER: PRJEB53216 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR9833020.fastq.gz	Fastqsanger.gz
	ERR9833030.fastq.gz	Fastqsanger.gz
	ERR9833050.fastq.gz	Fastqsanger.gz
	ERR9833060.fastq.gz	Fastqsanger.gz
	ERR9833070.fastq.gz	Fastqsanger.gz

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Transient upregulation of IRF1 during exit from naive pluripotency confers viral protection

Project description:Stem cells intrinsically express a subset of genes which are normally associated with interferon stimulation and the innate immune response. However, expression of these interferon stimulated genes (ISG) in stem cells is independent from external stimuli such as viral infection. Here, we show that the interferon regulatory factor 1, Irf1, is directly controlled by the murine formative pluripotency gene regulatory network and transiently upregulated during the transition from naive to formative pluripotency. IRF1 binds to regulatory regions of a conserved set of ISGs and is required for their faithful expression upon exit from naive pluripotency. We show that in the absence of IRF1, cells exiting the naive pluripotent stem cell state are more susceptible to viral infection. Irf1 therefore acts as a link between the formative pluripotency network, regulation of innate immunity genes and defense against viral infections during formative pluripotency.

| S-SCDT-EMBOR-2022-55375V1 | biostudies-other

Transient upregulation of IRF1 during exit from naive pluripotency confers viral protection.

Project description:Stem cells intrinsically express a subset of genes which are normally associated with interferon stimulation and the innate immune response. However, the expression of these interferon-stimulated genes (ISG) in stem cells is independent from external stimuli such as viral infection. Here, we show that the interferon regulatory factor 1, Irf1, is directly controlled by the murine formative pluripotency gene regulatory network and transiently upregulated during the transition from naive to formative pluripotency. IRF1 binds to regulatory regions of a conserved set of ISGs and is required for their faithful expression upon exit from naive pluripotency. We show that in the absence of IRF1, cells exiting the naive pluripotent stem cell state are more susceptible to viral infection. Irf1 therefore acts as a link between the formative pluripotency network, regulation of innate immunity genes, and defense against viral infections during formative pluripotency.

| S-EPMC9442322 | biostudies-literature

Asynchrony in the Exit from Naive Pluripotency

Project description:The asynchrony in the exit from naive pluripotency cannot be explained by differences in the cell cycle phase

| PRJEB68338 | ENA

STAT1 and IRF1 enrichment in naive and primed HeLa cells upon IFNγ treatment

Project description:STAT1 and IRF1 transcription factor enrichment by CUT&RUN. HeLa cells were primed with IFNγ for 24 hours, followed with IFNγ washout. After 48h, naïve and primed cells were induced by IFNγ for 1h and 3h. Cells were harvested at indicated time points and processed for CUT&RUN

2023-05-06 | E-MTAB-12625 | biostudies-arrayexpress

Asynchrony in the Exit from Naive Pluripotency (2024)

Project description:The asynchrony in the exit from naive pluripotency cannot be explained by differences in the cell cycle phase

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DNA methylation shapes the Polycomb landscape during the exit from naive pluripotency

Project description:DNA methylation shapes the Polycomb landscape during the exit from naive pluripotency

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STAT1 and IRF1 enrichment in naive and primed HeLa cells upon IFNγ treatment

Project description:STAT1 and IRF1 enrichment in naive and primed HeLa cells upon IFNγ treatment

| PRJEB59934 | ENA

The macrophage IRF8-IRF1 regulome is required for protection against infections, and is associated with chronic inflammation (RNA-Seq)

Project description:IRF8 and IRF1 are transcriptional regulators that play critical roles in the development and function of myeloid cells, including activation of macrophages by pro-inflammatory signals such as interferon gamma. Loss of IRF8 or IRF1 function causes severe susceptibility to infections in mice and in humans. We used chromatin immunoprecipitation sequencing and RNA sequencing in wild type, and in IRF8 and IRF1 mutant primary macrophages to systematically catalog all the genes bound by (cistromes) and transcriptionally activated (regulomes) by IRF8, IRF1, PU.1 and STAT1 including modulation of epigenetic histone marks. Of seven binding combinations identified, two (cluster 1: IRF8/IRF1/STAT1/PU.1; cluster 5: IRF1/STAT1/PU.1) were found to have a major role in controlling macrophage transcriptional programs both at basal level and following IFNγ activation. They direct expression of a set of genes, the IRF8/IRF1 regulome, that play critical roles in host inflammatory and anti-microbial defenses in mouse models of neuroinflammation and of pulmonary tuberculosis, respectively. In addition, this IRF8/IRF1 regulome is enriched for genes mutated in human primary immuno-deficiencies, and with loci associated for several inflammatory diseases in humans.

2016-03-07 | GSE77885 | GEO

The macrophage IRF8-IRF1 regulome is required for protection against infections, and is associated with chronic inflammation (ChIP-Seq)

2016-03-07 | GSE77884 | GEO

Oncogenic Ras inhibits IRF1 to promote viral oncolysis

Project description:Oncolytic viruses exploit common molecular changes in cancer cells, which are not present in normal cells, to target and kill cancer cells. Ras transformation and defects in type I interferon (IFN)-mediated antiviral responses are known to be the major mechanisms underlying viral oncolysis. Previously, we demonstrated that oncogenic RAS/Mitogen-activated protein kinase kinase (Ras/MEK) activation suppresses the transcription of many IFN-inducible genes in human cancer cells, suggesting that Ras transformation underlies type I IFN defects in cancer cells. Here, we investigated how Ras/MEK downregulates IFN-induced transcription. By conducting promoter deletion analysis of IFN-inducible genes, namely guanylate-binding protein 2 and IFN gamma inducible protein 47 (Ifi47), we identified the IFN regulatory factor 1 (IRF1) binding site as the promoter region responsible for the regulation of transcription by MEK. MEK inhibition promoted transcription of the IFN-inducible genes in wild type mouse embryonic fibroblasts (MEFs), but not in IRF1?/? MEFs, showing that IRF1 is involved in MEK-mediated downregulation of IFN-inducible genes. Furthermore, IRF1 protein expression was lower in RasV12 cells compared with vector control NIH3T3 cells, but was restored to equivalent levels by inhibition of MEK. Similarly, the restoration of IRF1 expression by MEK inhibition was observed in human cancer cells. IRF1 re-expression in human cancer cells caused cells to become resistant to infection by the oncolytic vesicular stomatitis virus strain. Together, this work demonstrates that Ras/MEK activation in cancer cells downregulates transcription of IFN-inducible genes by targeting IRF1 expression, resulting in increased susceptibility to viral oncolysis. RNA was isolated from RasV12 transformed NIH/3T3 cells (RasV12 cells) treated with 20?M U0126 or 500U/ml IFN-?, or left untreated, for 6 hours, triplicate biological samples (9 samples).

2014-11-13 | E-GEOD-49469 | biostudies-arrayexpress

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