STING-dependent antiviral innate immunity in multiple Drosophila species
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB72191 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR14335000_1.fastq.gz | Fastqsanger.gz | |||
| ERR14335000_2.fastq.gz | Fastqsanger.gz | |||
| ERR14335001_1.fastq.gz | Fastqsanger.gz | |||
| ERR14335001_2.fastq.gz | Fastqsanger.gz | |||
| ERR14335002_1.fastq.gz | Fastqsanger.gz |
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Project description:The cGAS (cyclic GMP-AMP synthase) -STING (Stimulator of interferon genes) pathway plays a central role in antiviral innate immunity in vertebrates. Recent studies have shown that invertebrates possess a related cGLR (cGAS-like receptor)-STING pathway. However, due to the lack of direct evidence demonstrating viral evasion of cGLR-STING-mediated immunity, the functional importance of cGLR-STING pathway in antiviral responses remains uncertain in invertebrates. Here, we show that an insect picorna-like virus CrPV (Cricket Paralysis virus) inhibits STING-mediated antiviral activity by altering the transcription start site of STING. Mechanistically, CrPV infection down-regulates several spliceosomal genes and disrupts pre-mRNA splicing. This splicing impairment is sufficient to stall RNA polymerase II in transcriptional initiation condensates, reduce global transcription efficiency, and reprogram the transcription start site of STING. Such a shift diverts STING expression from a functional antiviral isoform to a non-antiviral variant that partially suppresses STING activity, thereby disabling the cGLR-STING pathway. Our findings uncover an unconventional viral immune evasion strategy and an unexpected link between splicing suppression and STING-mediated antiviral response. Given the evolutionary conservation of splicing mechanisms and STING-like pathways, this mechanism may represent a broadly applicable regulatory principle in immune defense across species.
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Project description:The cGAS (cyclic GMP-AMP synthase) -STING (Stimulator of interferon genes) pathway plays a central role in antiviral innate immunity in vertebrates. Recent studies have shown that invertebrates possess a related cGLR (cGAS-like receptor)-STING pathway. However, due to the lack of direct evidence demonstrating viral evasion of cGLR-STING-mediated immunity, the functional importance of cGLR-STING pathway in antiviral responses remains uncertain in invertebrates. Here, we show that an insect picorna-like virus CrPV (Cricket Paralysis virus) inhibits STING-mediated antiviral activity by altering the transcription start site of STING. Mechanistically, CrPV infection down-regulates several spliceosomal genes and disrupts pre-mRNA splicing. This splicing impairment is sufficient to stall RNA polymerase II in transcriptional initiation condensates, reduce global transcription efficiency, and reprogram the transcription start site of STING. Such a shift diverts STING expression from a functional antiviral isoform to a non-antiviral variant that partially suppresses STING activity, thereby disabling the cGLR-STING pathway. Our findings uncover an unconventional viral immune evasion strategy and an unexpected link between splicing suppression and STING-mediated antiviral response. Given the evolutionary conservation of splicing mechanisms and STING-like pathways, this mechanism may represent a broadly applicable regulatory principle in immune defense across species.
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Project description:The innate immune cGAS-STING pathway is activated by cytosolic doubled-stranded DNA (dsDNA) to induce type I interferon response, which is essential for antiviral and antitumor immunity. However, intrinsic STING activation during viral infection or within the tumor microenvironment is often insufficient to achieve complete viral clearance or tumor regression, indicating the presence of additional mechanisms that evades its activity. Here, we identified COX2/PGE2 as an intrinsic negative regulator of STING activation, particularly in response to cytosolic mitochondrial DNA (mtDNA) generated during HSV-1 infection. Mechanistically, we demonstrated that PGE2 signals through the EP4-PKA axis to induce mitophagy and facilitate the clearance of immunostimulatory cytosolic mtDNA, thereby dampening STING-mediated antiviral response. Furthermore, we discovered STOML2 as a direct downstream target of PKA, thereby linking mitochondrial quality control to innate immune signaling. Together, our findings established the COX2/PGE2/PKA axis as an intrinsic negative regulator of STING signaling, which may be targeted to potentiate STING-mediated antiviral and antitumor immunity.
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