Evidence map›Paper›PMID 22102828›Full record

ArticlePLoS genetics2011

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

Sylvia E J Fischer, Taiowa A Montgomery, Chi Zhang, Noah Fahlgren, Peter C Breen, Alexia Hwang, Christopher M Sullivan, James C Carrington, Gary Ruvkun

Abstract read
In one paragraph

Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

61 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Intraspecific variation in the duration of epigenetic inheritance.bioRxiv : the preprint server for biology · 2025
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  14. Article
  15. bioRxiv : the preprint server for biology · 2024
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Sylvia E J FischerDepartment of Molecular Biology, Massachusetts General Hospital, Department of Genetics, Harvard Medical School, Boston, Massachusetts, United States of America.
Taiowa A Montgomery
Chi Zhang
Noah Fahlgren
Peter C Breen
Alexia Hwang
Christopher M Sullivan
James C Carrington
Gary Ruvkun

Funding

CONTROL OF THE C ELEGANS LINEAGE BY HETEROCHRONIC GENESR01GM044619 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI GARY B RUVKUN · 1991 to 2026
$14.5M
Genetic Analysis of RNA Virus-Host InteractionR37AI043288 · NIAID · OREGON STATE UNIVERSITY · PI CARRINGTON, JAMES C · 2008 to 2017
$3.1M
NIAID NIH HHS R37 AI043288NIGMS NIH HHS GM44619NIGMS NIH HHS R01 GM044619
6 · The paper itself

Abstract

Endogenous small interfering RNAs (siRNAs) are a class of naturally occuring regulatory RNAs found in fungi, plants, and animals. Some endogenous siRNAs are required to silence transposons or function in chromosome segregation; however, the specific roles of most endogenous siRNAs are unclear. The helicase gene eri-6/7 was identified in the nematode Caenorhabditis elegans by the enhanced response to exogenous double-stranded RNAs (dsRNAs) of the null mutant. eri-6/7 encodes a helicase homologous to small RNA factors Armitage in Drosophila, SDE3 in Arabidopsis, and Mov10 in humans. Here we show that eri-6/7 mutations cause the loss of 26-nucleotide (nt) endogenous siRNAs derived from genes and pseudogenes in oocytes and embryos, as well as deficiencies in somatic 22-nucleotide secondary siRNAs corresponding to the same loci. About 80 genes are eri-6/7 targets that generate the embryonic endogenous siRNAs that silence the corresponding mRNAs. These 80 genes share extensive nucleotide sequence homology and are poorly conserved, suggesting a role for these endogenous siRNAs in silencing of and thereby directing the fate of recently acquired, duplicated genes. Unlike most endogenous siRNAs in C. elegans, eri-6/7-dependent siRNAs require Dicer. We identify that the eri-6/7-dependent siRNAs have a passenger strand that is ∼19 nt and is inset by ∼3-4 nts from both ends of the 26 nt guide siRNA, suggesting non-canonical Dicer processing. Mutations in the Argonaute ERGO-1, which associates with eri-6/7-dependent 26 nt siRNAs, cause passenger strand stabilization, indicating that ERGO-1 is required to separate the siRNA duplex, presumably through endonucleolytic cleavage of the passenger strand. Thus, like several other siRNA-associated Argonautes with a conserved RNaseH motif, ERGO-1 appears to be required for siRNA maturation.

Indexed as

Gene SilencingAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsDNA HelicasesGene DuplicationGene Expression RegulationMutationOocytesPseudogenesRibonuclease IIIRNA-Binding ProteinsRNA, Double-StrandedRNA, Small InterferingCaenorhabditis elegans ProteinsDNA HelicasesERGO-1 protein, C elegansERI-6 protein, C elegansRibonuclease IIIRNA-Binding ProteinsRNA, Double-StrandedRNA, Small Interfering

Identifiers

PMID22102828
PMCPMC3213143

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.