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Nuclear RPSA triggers R-loop accumulation to induce cell death against RNA viral infection [DRIP-seq]

ABSTRACT: Nuclear RPSA triggers R-loop accumulation to induce cell death against RNA viral infection [DRIP-seq]

PROVIDER: PRJNA1281003 | ENA |

REPOSITORIES: ENA

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Nuclear RPSA triggers R-loop accumulation to induce cell death against RNA viral infection [DRIP-seq]

Project description:While RNA viruses evade host immune responses by perturbing transcriptional and translational machinery, the host organism counteracts viral invasion through activation of regulated cell death pathways. However, the precise molecular mechanisms underlying host-initiated cell death activation in response to viral infection remain poorly characterized. By genome-wide screening, we identified ribosomal protein RPSA as a broad inducer of RNA virus replication-dependent cell death that confers antiviral protection. Rpsa conditional knockout mice exhibited heightened susceptibility to RNA viruses with attenuated cell death activation in infected tissues. Mechanistically, RNA virus infection triggers K29-linked polyubiquitination of RPSA, which strengthens its binding to the helicase domain of NAT10 and potently inhibits NAT10's helicase activity, thereby blocking R-loop resolution. The resulting R-loop accumulation drives DNA damage-mediated cell death execution. Our findings uncover a novel intranuclear "inside-out" R-loop-driven cell death pathway orchestrated by RPSA, providing fresh insights into virus-host interactions and identifying potential therapeutic targets for RNA viral infections.

2025-07-18 | GSE300469 | GEO

Nuclear RPSA triggers R-loop accumulation to induce cell death against RNA viral infection

2025-07-18 | GSE300291 | GEO

Nuclear RPSA triggers R-loop accumulation to induce cell death against RNA viral infection

Project description:Nuclear RPSA triggers R-loop accumulation to induce cell death against RNA viral infection

| PRJNA1280040 | ENA

Detect R-loop signal by DRIP-seq in PA1 cell line

Project description:DRIP-seq of PA1 cells

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Ribosome protein RPSA promotes the expression of proinflammatory cytokines induced by HSV-1 infection

Project description:After HSV-1 infection, ribosomal protein RPSA can recognize viral DNA. To further verify the biological function of RPSA, we constructed the RPSA-deficient RAW264.7 macrophage cell line with the inducible CRISPR-Cas9 system, then found that the deletion of RPSA could effectively reduce the expression of proinflammatory cytokines such as IL-1α, IL-1β, IL-6, IL-12 and TNFα induced by HSV-1 infection.

2023-11-12 | GSE204893 | GEO

Ribosomal Protein SA (RPSA) is required for localized translation and sarcomere maintenance

Project description:Cardiomyocyte sarcomeres contain localized ribosomes, but the factors responsible for their localization and the significance of localized translation are unknown. Using proximity labeling, we identified Ribosomal Protein SA (RPSA) as a Z-line protein. In cultured cardiomyocytes, the loss of RPSA led to impaired local protein translation and reduced sarcomere integrity. By employing CAS9 expression mice along with adeno-associated viruses expressing CRE recombinase and single-guide RNAs targeting Rpsa, we knocked out RPSA in vivo and observed mis-localization of ribosomes and diminished local translation. These genetic mosaic mice with RPSA knockout in a subset of cardiomyocytes developed dilated cardiomyopathy, featuring atrophy of RPSA-deficient cardiomyocytes, compensatory hypertrophy of unaffected cardiomyocytes, left ventricular dilation, and impaired contractile function. We demonstrate that RPSA C-terminal domain is sufficient for localization Z-lines. These findings highlight RPSA as a ribosomal factor responsible for ribosome localization to the Z-line, facilitating local translation and sarcomere maintenance.

2024-06-04 | PXD046385 | Pride

ATAC-seq analysis in Rpsa-iKO RAW264.7 cells after HSV-1 infection

Project description:After HSV-1 infection, ribosomal protein RPSA can recognize viral DNA and promotes the expression of proinflammatory cytokines. Through ATAC-seq, we found that chromatin accessibility around transcription start sites (TSS) of proinflammatory cytokinse in HSV-1 infected Rpsa-iKO RAW264.7 was significantly reduced

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Deficiency of Rpsa results in reduced levels of H3K4me3 in inflammatory cytokines promoter regions

Project description:After HSV-1 infection, ribosomal protein RPSA can recognize viral DNA and promotes the expression of proinflammatory cytokines. Through ChIP-seq, we found that the level of H3K4me3 in proinflammatory cytokines(Il1b, Il6, Il12b, etc.) promoter regions was decreased due to Rpsa deficiency.

2023-11-12 | GSE204890 | GEO

DRIP-sequencing U2OS

Project description:DRIP-sequencing U2OS

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Interferon-dependent R-loop Induction by Zika Virus Contributes to Growth Attenuation [U251 DRIP-Seq]

Project description:Zika virus (ZIKV) infection in human neural progenitors triggers DNA damage and activates DNA damage response, leading to cell cycle arrest that can retard brain development. Here we link the ZIKV- induced S phase arrest to replication fork stalling and R-loop induction. DRIP-seq reveals that ZIKV infection induces R-loops at specific loci strongly enriched in the interferon-stimulated genes (ISGs). Bru-seq results further indicate that nascent ISGs transcripts are prone to R-loop induction upon infection. Knockout of interferon receptor eliminated the R-loops on ISGs and partially rescued S phase arrest in infected cells. And overexpression of RNaseH1 reduced ZIKV-mediated DNA damage and cell cycle arrest. We conclude that unscheduled expression of ISGs induced by ZIKV alters R-loop homeostasis and perturbs replication fork progression, leading to fork stalling and eventually DNA damage. IFN- dependent R-loop induction represents a previously unknown, nucleic acid-based mechanism for cell cycle arrest.

2025-05-29 | GSE274207 | GEO

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