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Stabilization of mitochondrial double stranded RNAs by SLIRP promotes positive feedback amplification of antiviral signaling.

ABSTRACT: Stabilization of mitochondrial double stranded RNAs by SLIRP promotes positive feedback amplification of antiviral signaling.

PROVIDER: PRJNA1043122 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26894774_1.fastq.gz	Fastqsanger.gz
	SRR26894774_2.fastq.gz	Fastqsanger.gz
	SRR26894775_1.fastq.gz	Fastqsanger.gz
	SRR26894775_2.fastq.gz	Fastqsanger.gz
	SRR26894776_1.fastq.gz	Fastqsanger.gz

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Stabilization of mitochondrial double stranded RNAs by SLIRP promotes positive feedback amplification of antiviral signaling.

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

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AXIN1 boosts antiviral response through IRF3 stabilization and induced phase separation

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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.

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Project description:The antiviral nuclear body protein SP140 represses Ifnb1 transcript stabilization by the novel regulator RESIST [RNA-seq]

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