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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

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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

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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.

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R-loop landscapes in Rice (Oryza sativa) [DRIP-seq]

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

Project description:DRIP-seq of PA1 cells

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Human and mouse DRIP-seq and DRIPc-seq

Project description:This study profiles RNA:DNA hybrid formation in human and mouse cell lines. DRIPc-seq (strand-specific R-loop mapping) was performed on human NT2 cells and mouse 3T3 cells. DRIP-seq (R-loop mapping) was performed on human NT2 and K562 and mouse E14 and 3T3 cell lines. MethylC-seq and RNA-seq were performed on NT2.

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Disruption of RNAPII transcription elongation links Oncogenic splicing factor mutations to replciation stress and targetable alterations in chromatin landscape [DRIP-seq]

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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.

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