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An endogenous retrovirus regulates tumor-specific expression of the immune transcriptional regulator SP140 [RNA-seq]

ABSTRACT: An endogenous retrovirus regulates tumor-specific expression of the immune transcriptional regulator SP140 [RNA-seq]

PROVIDER: PRJNA1077371 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27996659_1.fastq.gz	Fastqsanger.gz
	SRR27996659_2.fastq.gz	Fastqsanger.gz
	SRR27996660_1.fastq.gz	Fastqsanger.gz
	SRR27996660_2.fastq.gz	Fastqsanger.gz
	SRR27996661_1.fastq.gz	Fastqsanger.gz

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An endogenous retrovirus regulates tumor-specific expression of the immune transcriptional regulator SP140 [CUT&RUN]

Project description:Speckled Protein 140 (SP140) is a chromatin reader with critical roles regulating immune cell transcriptional programs, and SP140 splice variants are associated with immune diseases including Crohn’s disease, multiple sclerosis, and chronic lymphocytic leukemia. SP140 expression is currently thought to be restricted to immune cells. However, by analyzing human transcriptomic datasets from a wide range of normal and cancer cell types, we found recurrent cancer-specific expression of SP140, driven by an alternative intronic promoter derived from an intronic endogenous retrovirus (ERV). The ERV belongs to the primate-specific LTR8B family. The ERV drives expression of multiple cancer-specific isoforms, including a nearly full-length isoform that retains all the functional domains of the full-length canonical isoform and is also localized within the nucleus, consistent with a role in chromatin regulation. In a fibrosarcoma cell line, silencing the cancer-specific ERV promoter of SP140 resulted in increased sensitivity to interferon-mediated cytotoxicity and dysregulation of multiple genes. Our findings implicate aberrant ERV-mediated SP140 expression as a novel mechanism contributing to immune gene dysregulation in a wide range of cancer cells.

2024-02-20 | GSE256010 | GEO

An endogenous retrovirus regulates tumor-specific expression of the immune transcriptional regulator SP140 [RNA-seq]

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An endogenous retrovirus regulates tumor-specific expression of the immune transcriptional regulator SP140

Project description:An endogenous retrovirus regulates tumor-specific expression of the immune transcriptional regulator SP140

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An endogenous retrovirus regulates tumor-specific expression of the immune transcriptional regulator SP140 [CUT&RUN]

Project description:An endogenous retrovirus regulates tumor-specific expression of the immune transcriptional regulator SP140 [CUT&RUN]

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An endogenous retrovirus regulates tumor-specific expression of the immune transcriptional regulator SP140

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

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m6A methylation regulates the fate of endogenous retrovirus transcripts

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The antiviral nuclear body protein SP140 represses Ifnb1 transcript stabilization by the novel regulator RESIST [WT and SP140 KO RNA-seq]

Project description:Negative regulation of the antiviral cytokine IFN-I is critical to prevent host pathology, but is not fully understood. The highly conserved but understudied epigenetic reader and nuclear body protein SP140 represses IFN-I by an unknown mechanism. We describe the mechanism by which SP140 negatively regulates IFN-I, and include RNA-seq data of WT (B6) and SP140 KO BMMs untreated or treated with 100 ug/mL DMXAA for 8 hours in this dataset. We found that SP140 represses the expression of a novel positive regulator of IFN-I previously annotated as an annexin II receptor, which we rename RESIST (REgulated Stimulator of IFN-I via Stabilization of Transcript). RESIST promotes IFN-I mRNA stability by binding the CCR4-NOT mRNA deadenylase complex and blocking recruitment of the TTP family of RNA-binding proteins, which negatively regulate IFN-I mRNA stability, to CCR4-NOT. Mechanistically, RESIST uses N and C-terminal alpha-helices respectively to either dock to the CCR4-NOT complex or block TTP family binding. Our work reveals a new regulator of IFN-I and a new mechanism regulating IFN-I mRNA stability.

2024-08-28 | GSE269808 | GEO

The antiviral nuclear body protein SP140 represses Ifnb1 transcript stabilization by the novel regulator RESIST

Project description:Negative regulation of the antiviral cytokine IFN-I is critical to prevent host pathology, but is not fully understood. The highly conserved but understudied epigenetic reader and nuclear body protein SP140 represses IFN-I by an unknown mechanism. We describe the mechanism by which SP140 negatively regulates IFN-I, and include CUT&RUN data in this dataset. We performed anti-HA CUT&RUN on SP140KO macrophages transduced with HA-tagged or untagged SP140. We found that SP140 represses the expression of a novel positive regulator of IFN-I previously annotated as an annexin II receptor, which we rename RESIST (REgulated Stimulator of IFN-I via Stabilization of Transcript). RESIST promotes IFN-I mRNA stability by binding the CCR4-NOT mRNA deadenylase complex and blocking recruitment of the TTP family of RNA-binding proteins, which negatively regulate IFN-I mRNA stability, to CCR4-NOT. Mechanistically, RESIST uses N and C-terminal alpha-helices respectively to either dock to the CCR4-NOT complex or block TTP family binding. We also find SP140 does not bind the Ifnb1 gene itself. Consistent with previous results, SP140 binds genes involved in embryonic development. Our work reveals a new regulator of IFN-I and a new mechanism regulating IFN-I mRNA stability.

2024-08-28 | GSE269315 | GEO

Cryptic endogenous retrovirus subfamilies in the primate lineage

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The antiviral nuclear body protein SP140 represses Ifnb1 transcript stabilization by the novel regulator RESIST [ATAC-seq]

Project description:Negative regulation of the antiviral cytokine IFN-I is critical to prevent host pathology, but is not fully understood. The highly conserved but understudied epigenetic reader and nuclear body protein SP140 represses IFN-I by an unknown mechanism. We describe the mechanism by which SP140 negatively regulates IFN-I, and include ATAC-seq data of WT (B6) and SP140 KO BMMs untreated or treated with 100 ug/mL DMXAA for 8 hours in this dataset. We found that SP140 represses the expression of a novel positive regulator of IFN-I previously annotated as an annexin II receptor, which we rename RESIST (REgulated Stimulator of IFN-I via Stabilization of Transcript). RESIST promotes IFN-I mRNA stability by binding the CCR4-NOT mRNA deadenylase complex and blocking recruitment of the TTP family of RNA-binding proteins, which negatively regulate IFN-I mRNA stability, to CCR4-NOT. Mechanistically, RESIST uses N and C-terminal alpha-helices respectively to either dock to the CCR4-NOT complex or block TTP family binding. Our work reveals a new regulator of IFN-I and a new mechanism regulating IFN-I mRNA stability.

2024-08-28 | GSE269811 | GEO

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