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Transcriptome Regulation by PARP13 in Basal and Antiviral States in Human Cells

ABSTRACT: Transcriptome Regulation by PARP13 in Basal and Antiviral States in Human Cells

PROVIDER: PRJNA889426 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21863800_1.fastq.gz	Fastqsanger.gz
	SRR21863800_2.fastq.gz	Fastqsanger.gz
	SRR21863801_1.fastq.gz	Fastqsanger.gz
	SRR21863801_2.fastq.gz	Fastqsanger.gz
	SRR21863794_1.fastq.gz	Fastqsanger.gz

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Transcriptome Regulation by PARP13 in Basal and Antiviral States in Human Cells (eCLIP)

Project description:The RNA-binding protein PARP13 is a primary factor in the innate antiviral response. PARP13 can suppress translation and drive decay of bound viral and host RNA. PARP13 interacts with many proteins encoded by interferon-stimulated genes (ISG) to perform its antiviral activities, such as activation of the pathway mediated by post-translational addition ISG15 or ISGylation. The RNA-binding domains of both PARP13 and its primary cofactor, TRIM25, are required for antiviral activity. Here we perform enhanced crosslinking immunoprecipitation (eCLIP) and RNA-seq to investigate the role of PARP13 expression and RNA binding in transcriptome regulation within human cells. We find that PARP13 regulates the transcriptome in basal and antiviral states and that the antiviral response shifts PARP13 target localization, but not its binding preferences. We demonstrate that PARP13 expression supports the expression of ISGylation-related genes, including TRIM25. Using the common targets PARP13 and TRIM25 share, we assess their spatial relationship along transcripts and show that PARP13 and TRIM25 associate in part via RNA-protein interactions. Evidence from genomic data and molecular biology experiments provide insight into the geometry of PARP13's interface with its cofactor TRIM25 and implicates PARP13 in creating and maintaining a cellular environment poised for an antiviral response.

2023-09-11 | GSE215250 | GEO

Transcriptome Regulation by PARP13 in Basal and Antiviral States in Human Cells (eCLIP)

Project description:Transcriptome Regulation by PARP13 in Basal and Antiviral States in Human Cells (eCLIP)

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Transcriptome regulation by PARP13 in basal and antiviral states in human cells.

Project description:The RNA-binding protein PARP13 is a primary factor in the innate antiviral response, which suppresses translation and drives decay of bound viral and host RNA. PARP13 interacts with many proteins encoded by interferon-stimulated genes (ISG) to activate antiviral pathways including co-translational addition of ISG15, or ISGylation. We performed enhanced crosslinking immunoprecipitation (eCLIP) and RNA-seq in human cells to investigate PARP13's role in transcriptome regulation for both basal and antiviral states. We find that the antiviral response shifts PARP13 target localization, but not its binding preferences, and that PARP13 supports the expression of ISGylation-related genes, including PARP13's cofactor, TRIM25. PARP13 associates with TRIM25 via RNA-protein interactions, and we elucidate a transcriptome-wide periodicity of PARP13 binding around TRIM25. Taken together, our study implicates PARP13 in creating and maintaining a cellular environment poised for an antiviral response through limiting PARP13 translation, regulating access to distinct mRNA pools, and elevating ISGylation machinery expression.

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Transcriptome Regulation by PARP13 in Basal and Antiviral States in Human Cells

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

2023-09-11 | GSE215251 | GEO

Lockdown, caregiving, and antiviral gene regulation in macaques

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Project description:Poly(ADP-ribose) Polymerase-13 (PARP13/ZAP/ZC3HAV1) is an antiviral factor, active against specific RNA viruses such as MLV, SINV and HIV. During infection PARP13 binds viral RNA via its 4 CCCH-type zinc finger domains and targets it for degradation by recruiting cellular mRNA decay factors such as the exosome complex and XRN1. Here we show that PARP13 binds to and regulates cellular mRNA under physiological conditions. Knock-down of PARP13 via RNAi results in the misregulation of hundreds of transcripts with an enrichment in signal peptide containing proteins. Among the most upregulated transcripts is TRILR4

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Project description:Previous research has linked perceived social isolation (loneliness) to reduced antiviral immunity, but the immunologic effects of the objective social isolation imposed by pandemic “shelter in place” (SIP) policies is unknown. We assessed the immunologic impact of SIP by relocating 21 adult male rhesus macaques from 2000 sq-m field cage communities of 70-132 other macaques to 2 wks of individual housing in indoor shelters. SIP was associated with down-regulation of Type I interferon (IFN) antiviral gene expression. This effect emerged within the first 48 hrs of SIP, persisted for at least 2 wks, and abated within 4 wks of return to social housing. A subsequent round of SIP in the presence of a novel juvenile macaque abrogated this effect. These results identify a significant adverse effect of SIP social isolation on antiviral immune regulation in circulating immune cells and they suggest a potential behavioral strategy for ameliorating such effects by promoting pro-social engagement during SIP.

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