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Caenorhabditis elegans ADAR editing and the ERI-6/7/MOV10 RNAi pathway silence endogenous viral elements and LTR retrotransposons

ABSTRACT: To examine the roles of the ADAR genes and the ERI-6/7 helicase in endogenous RNAi pathways, we sequenced small RNA of adr-1; adr-2; eri-6 mutants. We also analyzed the transcriptomes of these mutants using total RNAseq and mRNAseq. mRNAseq was done in mutants depleted for the RNAi factors drh-1 and nrde-3, or control RNAi

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE143595 | GEO | 2020/01/14

REPOSITORIES: GEO

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The ERI-6/7 helicase acts at the first stage of an siRNA amplification pathway that targets recent gene duplications.

Project description:To characterize the role of the ERI-6/7 helicase in endogenous small RNA pathways in C. elegans, small RNA populations from null alleles of eri-6 and eri-7, and from mutants of known endogenous RNAi pathway factors, eri-1 and ergo-1, were determined by deep sequencing, and compared to wild type.

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Caenorhabditis elegans ADAR editing and the ERI-6/7/MOV10 RNAi pathway silence endogenous viral elements and LTR retrotransposons

Project description:Caenorhabditis elegans ADAR editing and the ERI-6/7/MOV10 RNAi pathway silence endogenous viral elements and LTR retrotransposons

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Transcriptome analysis of C. elegans embryos lacking ADARs and the 26G pathway

Project description:Adenosine deaminases that act on RNA (ADARs) catalyze the conversion of adenosine to inosine in dsRNA. C. elegans ADARs, ADR-1 and ADR-2, promote the expression of genes containing dsRNA structures by preventing their processing into siRNAs and silencing by RNAi. The 26G endogenous siRNA (endo-siRNA) pathway generates a subset of siRNAs distinct from those made in adr-1;adr-2 mutants, but using many of the same factors. We found that adr-1;adr-2;rrf-3 mutants, lacking both ADARs and the RNA-dependent RNA polymerase RRF-3 required for the 26G pathway, display a bursting phenotype rescued by the RNAi factors RDE-1 and RDE-4. To determine what gene expression changes underlie the synthetic phenotype of adr-1;adr-2;rrf-3 mutants, we sequenced poly(A)+ RNA from adr-1;adr-2;rrf-3 embryos, their parent strains, and strains rescued with mutations in rde-1 and rde-4. We found that genes associated with edited structures were robustly downregulated in adr-1;adr-2;rrf-3 mutants in a manner partially dependent on rde-1 and rde-4. Additionally, genes induced during Orsay virus infections were induced in rrf-3 mutants and further upregulated in adr-1;adr-2;rrf-3 mutants, again dependent in part on rde-1 and rde-4.

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Caenorhabditis elegans ADAR editing and the ERI-6/7/MOV10 RNAi pathway silence endogenous viral elements and LTR retrotransposons.

Project description:Endogenous retroviruses and long terminal repeat (LTR) retrotransposons are mobile genetic elements that are closely related to retroviruses. Desilenced endogenous retroviruses are associated with human autoimmune disorders and neurodegenerative diseases. Caenorhabditis elegans and related Caenorhabditis spp. contain LTR retrotransposons and, as described here, numerous integrated viral genes including viral envelope genes that are part of LTR retrotransposons. We found that both LTR retrotransposons and endogenous viral elements are silenced by ADARs [adenosine deaminases acting on double-stranded RNA (dsRNA)] together with the endogenous RNA interference (RNAi) factor ERI-6/7, a homolog of MOV10 helicase, a retrotransposon and retrovirus restriction factor in human. siRNAs corresponding to integrated viral genes and LTR retrotransposons, but not to DNA transposons, are dependent on the ADARs and ERI-6/7. siRNAs corresponding to palindromic repeats are independent of the ADARs and ERI-6/7, and are in fact increased in adar- and eri-6/7-defective mutants because of an antiviral RNAi response to dsRNA. Silencing of LTR retrotransposons is dependent on downstream RNAi factors and P granule components but is independent of the viral sensor DRH-1/RIG-I and the nuclear Argonaute NRDE-3. The activation of retrotransposons in the ADAR- and ERI-6/7/MOV10-defective mutant is associated with the induction of the unfolded protein response (UPR), a common response to viral infection. The overlap between genes induced upon viral infection and infection with intracellular pathogens and genes coexpressed with retrotransposons suggests that there is a common response to different types of foreign elements that includes a response to proteotoxicity presumably caused by the burden of replicating pathogens and expressed retrotransposons.

| S-EPMC7084138 | biostudies-literature

The ERI-6/7 helicase acts at the first stage of an siRNA amplification pathway that targets recent gene duplications.

2011-09-25 | E-GEOD-32366 | biostudies-arrayexpress

Antisense ribosomal siRNAs inhibit RNA polymerase I-directed transcription in C. elegans

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2021-01-20 | GSE165078 | GEO

The C. elegans neural editome reveals an ADAR target mRNA required for proper chemotaxis

Project description:ADAR proteins alter gene expression both via catalyzing adenosine-to-inosine RNA editing and in an editing-independent manner by binding to target RNAs. Loss of ADARs affects neuronal function in all animals studied to date. To identify important neuronal targets in C. elegans, we performed the first unbiased assessment of the effects of ADR-2, the C. elegans editing enzyme, on the neural transcriptome. We identified the neural editome and gene expression changes associated with the loss of adr-2. As C. elegans lacking adr-2 exhibit reduced chemotaxis, our studies focused on targets that regulate this process. We identified an edited mRNA, clec-41, whose expression is dependent on ADR-2. Expressing clec-41 in adr-2 deficient neural cells restored chemotaxis. This study is the first of its kind in the RNA editing field to span from developing novel methodology for tissue-specific target identification to organismal behavior, significantly advancing our understanding of ADAR functions in neural cells.

2017-06-13 | GSE98869 | GEO

A Small-RNA-Mediated Feedback Loop Maintains Proper Levels of 22G-RNAs in C. elegans

Project description:ERI-6/7 is a negative regulator of exogenous RNAi, however the function of SOSI-1 has never previously been characterized. We noticed that expression of sosi-1 and eri-6/7 are mutually exclusive. Due to its genomic locus being nested within the eri-6 locus, we hypothesized that sosi-1 could be acting as a regulator of ERI-6/7 function by disrupting eri-6/7 expression upon sensing changes in the production of MUT-16-dependent 22G siRNAs. Our data confirms that expression of the sosi-1 mRNA is regulated by MUT-16-dependent 22G siRNAs. In addition, we show here that the expression of the eri-6 and eri-7 pre-mRNAs, and thus the eri-6/7 trans-spliced mRNA, are mis-regulated upon loss of sosi-1-targeting and eri-6[e-f]-targeting MUT-16-dependent 22G siRNAs, suggesting that sosi-1 and eri-6[e-f] act as a feedback sensor for small RNA function.

2020-05-21 | GSE145217 | GEO

Analysis of transgene siRNAs and ARL-8-dependent siRNAs in Caenorhabditis elegans

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2013-12-15 | E-GEOD-52785 | biostudies-arrayexpress

A nuclear Argonaute promotes germline immortality and epigenetic inheritance across generations

Project description:dsRNA-mediated gene silencing (RNAi) can be inherited for multiple generations in C. elegans. To understand this process we conducted a genetic screen for animals defective for transmitting RNAi silencing signals to future generations. This screen identified the gene heritable RNAi defective (hrde)-1. hrde-1 encodes an Argonaute (Ago) that associates with siRNAs in germ cells of the progeny of animals exposed to dsRNA. In nuclei of these germ cells, HRDE-1 engages the Nrde nuclear RNAi pathway to promote RNAi inheritance, and directs H3K9me3 chromatin marks at RNAi targeted genomic loci. Under normal growth conditions, HRDE-1 associates with endogenously expressed small RNAs, which direct nuclear gene silencing in germ cells. In RNAi inheritance mutant animals, silencing is lost over generational time. Concurrently, RNAi inheritance mutant animals exhibit progressively worsening germline defects that ultimately lead to sterility. These results establish that the Ago HRDE-1 directs gene-silencing events in germ cell nuclei, which are required for multi-generational RNAi inheritance and immortality of the germ cell lineage. We propose that C. elegans use the RNAi inheritance machinery to transmit epigenetic information, accrued by past generations, into future generations to ensure immortality of the germ cell lineage. H3K9me3 Chip-IP for C. elegans strains nrde-3, nrde-4, glp-4. Small RNA-seq for small RNAs co-immunoprecipitated with HRDE-1

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