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Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE41058 | GEO | 2013/06/01

SECONDARY ACCESSION(S): PRJNA175637

REPOSITORIES: GEO

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Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-06-01 | E-GEOD-41058 | biostudies-arrayexpress

Competition between virus-derived and endogenous small RNAs regulates gene expression in Caenorhabditis elegans.

Project description:Positive-strand RNA viruses encompass more than one-third of known virus genera and include many medically and agriculturally relevant human, animal, and plant pathogens. The nematode Caenorhabditis elegans and its natural pathogen, the positive-strand RNA virus Orsay, have recently emerged as a new animal model to understand the mechanisms and evolution of innate immune responses. In particular, the RNA interference (RNAi) pathway is required for C. elegans resistance to viral infection. Here we report the first genome-wide analyses of gene expression upon viral infection in C. elegans. Using the laboratory strain N2, we identify a novel C. elegans innate immune response specific to viral infection. A subset of these changes is driven by the RNAi response to the virus, which redirects the Argonaute protein RDE-1 from its endogenous small RNA cofactors, leading to loss of repression of endogenous RDE-1 targets. Additionally, we show that a C. elegans wild isolate, JU1580, has a distinct gene expression signature in response to viral infection. This is associated with a reduction in microRNA (miRNA) levels and an up-regulation of their target genes. Intriguingly, alterations in miRNA levels upon JU1580 infection are associated with a transformation of the antiviral transcriptional response into an antibacterial-like response. Together our data support a model whereby antiviral RNAi competes with endogenous small RNA pathways, causing widespread transcriptional changes. This provides an elegant mechanism for C. elegans to orchestrate its antiviral response, which may have significance for the relationship between small RNA pathways and immune regulation in other organisms.

| S-EPMC3730100 | biostudies-literature

Changes in small RNAs upon Viral infection of C.elegans

Project description:Attempt to identify small non-coding RNAs that change in levels as a result of viral infection of C.elegans

2013-06-01 | GSE41057 | GEO

Changes in small RNAs upon Viral infection of C.elegans

Project description:Attempt to identify small non-coding RNAs that change in levels as a result of viral infection of C.elegans Small non-coding RNA (18-30nt) was extracted from animals either infected with Orsay virus or uninfected as indicated.

2013-06-01 | E-GEOD-41057 | biostudies-arrayexpress

Analysis of small RNA response to viral infection in C.elegans

Project description:Dissection of the small RNA pathway required for generation of an antiviral small RNA response

2013-06-01 | GSE41693 | GEO

Interaction between endogenous microRNAs and virus-derived small RNAs controls viral replication in insect vectors.

Project description:MicroRNAs (miRNAs) play an important role in resisting virus infection in insects. Viruses are recognized by insect RNA interference systems, which generate virus-derived small RNAs (vsRNAs). To date, it is unclear whether viruses employ vsRNAs to regulate the expression of endogenous miRNAs. We previously found that miR-263a facilitated the proliferation of rice stripe virus (RSV) in the insect vector small brown planthopper. However, miR-263a was significantly downregulated by RSV. Here, we deciphered the regulatory mechanisms of RSV on miR-263a expression. The promoter region of miR-263a was characterized, and the transcription factor YY1 was found to negatively regulate the transcription of miR-263a. The nucleocapsid protein of RSV promoted the inhibitory effect of YY1 on miR-263a transcription by reducing the binding ability of RNA polymerase II to the promoter of miR-263a. Moreover, an RSV-derived small RNA, vsR-3397, downregulated miR-263a transcription by directly targeting the promoter region with partial sequence complementarity. The reduction in miR-263a suppressed RSV replication and was beneficial for maintaining a tolerable accumulation level of RSV in insect vectors. This dual regulation mechanism reflects an ingenious adaptation strategy of viruses to their insect vectors.

| S-EPMC9295959 | biostudies-literature

Analysis of small RNA response to viral infection in C.elegans

Project description:Dissection of the small RNA pathway required for generation of an antiviral small RNA response Small non-coding RNA (~15-30nt) was extracted from animals infected with the Orsay virus

2013-06-01 | E-GEOD-41693 | biostudies-arrayexpress

Viral suppressors of RNA silencing hinder exogenous and endogenous small RNA pathways in Drosophila.

Project description:BackgroundIn plants and insects, RNA interference (RNAi) is the main responder against viruses and shapes the basis of antiviral immunity. Viruses counter this defense by expressing viral suppressors of RNAi (VSRs). While VSRs in Drosophila melanogaster were shown to inhibit RNAi through different modes of action, whether they act on other silencing pathways remained unexplored.Methodology/principal findingsHere we show that expression of various plant and insect VSRs in transgenic flies does not perturb the Drosophila microRNA (miRNA) pathway; but in contrast, inhibits antiviral RNAi and the RNA silencing response triggered by inverted repeat transcripts, and injection of dsRNA or siRNA. Strikingly, these VSRs also suppressed transposon silencing by endogenous siRNAs (endo-siRNAs).Conclusions/significanceOur findings identify VSRs as tools to unravel small RNA pathways in insects and suggest a cosuppression of antiviral RNAi and endo-siRNA silencing by viruses during fly infections.

| S-EPMC2689938 | biostudies-literature

The RNA phosphatase PIR-1 regulates endogenous small RNA pathways in C. elegans.

Project description:Eukaryotic cells regulate 5'-triphosphorylated RNAs (ppp-RNAs) to promote cellular functions and prevent recognition by antiviral RNA sensors. For example, RNA capping enzymes possess triphosphatase domains that remove the γ phosphates of ppp-RNAs during RNA capping. Members of the closely related PIR-1 (phosphatase that interacts with RNA and ribonucleoprotein particle 1) family of RNA polyphosphatases remove both the β and γ phosphates from ppp-RNAs. Here, we show that C. elegans PIR-1 dephosphorylates ppp-RNAs made by cellular RNA-dependent RNA polymerases (RdRPs) and is required for the maturation of 26G-RNAs, Dicer-dependent small RNAs that regulate thousands of genes during spermatogenesis and embryogenesis. PIR-1 also regulates the CSR-1 22G-RNA pathway and has critical functions in both somatic and germline development. Our findings suggest that PIR-1 modulates both Dicer-dependent and Dicer-independent Argonaute pathways and provide insight into how cells and viruses use a conserved RNA phosphatase to regulate and respond to ppp-RNA species.

| S-EPMC7867642 | biostudies-literature

Competition for XPO5 binding between Dicer mRNA, pre-miRNA and viral RNA regulates human Dicer levels.

Project description:MicroRNAs (miRNAs) are a class of small, noncoding RNAs that function by regulating gene expression post-transcriptionally. Alterations in miRNA expression can strongly influence cellular physiology. Here we demonstrated cross-regulation between two components of the RNA interference (RNAi) machinery in human cells. Inhibition of exportin-5, the karyopherin responsible for pre-miRNA export, downregulated expression of Dicer, the RNase III required for pre-miRNA maturation. This effect was post-transcriptional and resulted from an increased nuclear localization of Dicer mRNA. In vitro assays and cellular RNA immunoprecipitation experiments showed that exportin-5 interacted directly with Dicer mRNA. Titration of exportin-5 by overexpression of either pre-miRNA or the adenoviral VA1 RNA resulted in loss of Dicer mRNA-exportin-5 interaction and reduction of Dicer level. This saturation also occurred during adenoviral infection and enhanced viral replication. Our study reveals an important cross-regulatory mechanism between pre-miRNA or viral small RNAs and Dicer through exportin-5.

| S-EPMC3595992 | biostudies-literature

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