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ADAR binding to dsRNA prevents exogenous RNAi from attacking self-produced dsRNA in C. elegans

ABSTRACT: The ability of an organism to distinguish between self and foreign dsRNA is central to eliciting an immune response when needed while preventing autoimmunity. Using Caenorhabditis elegans, we investigated the interplay between two host pathways that regulate dsRNA expression and function, A-to-I RNA editing by ADARs, and RNA interference (RNAi). We found that the number of siRNAs targeting edited genes is significantly upregulated in ADAR mutant animals. In addition, despite an almost complete depletion of primary siRNAs generated from editing sites in wild-type animals, secondary siRNAs are generated from edited transcripts, suggesting that ADARs antagonize only the first step of RNAi processing. We show that ADARs interfere with the efficacy of exogenous RNAi in vivo, likely to prevent trans-silencing, and provide evidence that ADR-2 binding to dsRNA is required for efficient RNAi suppression. This work sheds light on how RNA editing safeguards self dsRNAs against immune recognition and by-product degradation.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE239862 | GEO | 2026/09/24

REPOSITORIES: GEO

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dsRNAs expressed in C. elegans development

Project description:Cellular RNAs containing double-stranded RNA (dsRNA) structures are subject to A-to-I RNA editing by the adenosine deaminases that act on RNA (ADARs). While A-to-I editing can alter mRNA coding potential, most editing is observed in non-coding sequences, the function of which remains poorly characterized. Using a dsRNA immunoprecipitation and high-thoughput sequencing (dsRIP-Seq) approach, we identify 1523 expressed A-to-I edited regions and characterize their expression during Caenorhabditis elegans development. We observe that edited regions are highly expressed in early development and are closely associated with protein-coding genes. Edited dsRNA structures give rise to abundant small interfering RNAs (siRNAs) that are negatively correlated with ADAR expression and regulate the developmental expression of associated genes.

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The dsRBP and inactive editor, ADR-1, utilizes dsRNA binding to regulate A-to-I RNA editing across the C. elegans transcriptome

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ADAR1 regulates dsRNA formation in nuclear and mitochondrial transcripts through editing-dependent and -independent mechanisms

Project description:Endogenous (self) double-stranded RNAs (dsRNAs) in human cells can activate innate immune responses. ADAR1, an A-to-I editing enzyme of dsRNAs, suppresses aberrant immune activation by self-dsRNAs. However, how ADAR1 influences the cellular dsRNA landscape remains unclear. We show that human ADAR1 downregulates self-dsRNA abundance through editing-dependent and editing-independent mechanisms. We further conducted quantitative dsRNA-sequencing on wild-type and ADAR1-deficient cells. dsRNAs are enriched in protein-coding mRNAs − especially those with repetitive elements and elongated 3’UTRs − and mitochondrial RNAs. ADAR1 loss markedly increased dsRNA quantity but minimally impacted dsRNA identity. ADAR1-regulated dsRNA transcripts consist of nuclear-encoded mRNAs and, unexpectedly, mitochondria-encoded RNAs rarely edited by ADAR1. Accordingly, dsRNAs accumulate to high levels within the mitochondria of ADAR1-deficient cells. Notably, ADAR1 loss sensitizes cells to inflammation under mitochondrial stress (e.g., mitochondrial herniation, X-ray radiation). Hence, we show that dsRNAs regulated by ADAR1 go beyond A-to-I edited transcripts, and that ADAR1 can control mitochondrial-dsRNAs.

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ADARs affect the biogenesis of many small RNAs in C. elegans, but few mature small RNAs are edited

Project description:Adenosine deaminases that act on RNA (ADARs) are RNA editing enzymes that convert adenosine to inosine in double-stranded RNA (dsRNA). To evaluate effects of ADARs on small RNAs that derive from dsRNA precursors, we performed deep-sequencing, comparing small RNAs from wildtype and ADAR mutant C. elegans. While editing in small RNAs was rare, at least 40% of microRNAs had altered levels in at least one ADAR mutant strain, and miRNAs with significantly altered levels had mRNA targets with correspondingly affected levels. About 40% of siRNAs derived from endogenous genes (endo-siRNAs) also had altered levels in at least one mutant strain, including 63% of Dicer-dependent endo-siRNAs. The 26G class of endo-siRNAs was significantly affected by ADARs, and many altered 26G loci had intronic reads, and histone modifications associated with transcriptional silencing. Our data indicate ADARs, through both direct and indirect mechanisms, are important for maintaining wildtype levels of many small RNAs in C. elegans. Deep sequencing of small RNAs in wild-type (N2), adr-1 null, adr-2 null and adr-1;adr-2 null mixed stage C. elegans

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ADAR binding to dsRNA prevents exogenous RNAi from attacking self-produced dsRNA in C. elegans

Project description:ADAR binding to dsRNA prevents exogenous RNAi from attacking self-produced dsRNA in C. elegans

| PRJNA1001294 | ENA

The dsRBP and inactive editor, ADR-1, utilizes dsRNA binding to regulate A-to-I RNA editing across the C. elegans transcriptome

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