Evidence map›Paper›PMID 21253006›Full record

ArticlePloS one2010

Natural variation of the amino-terminal glutamine-rich domain in Drosophila argonaute2 is not associated with developmental defects.

Daniel Hain, Brian R Bettencourt, Katsutomo Okamura, Tibor Csorba, Wibke Meyer, Zhigang Jin, Jason Biggerstaff, Haruhiko Siomi, Gyorgy Hutvagner, Eric C Lai and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-weighted citation impact, top 14% of its field
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

25 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Polyglutamine Repeats in Viruses.Molecular neurobiology · 2019
    Review
  8. Article
  9. Review
  10. Article
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  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. The DNA virus Invertebrate iridescent virus 6 is a target of the Drosophila RNAi machinery.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
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

12 authors at 9 institutions in 4 countries.

Daniel HainDivision of Cell and Developmental Biology, College of Life Sciences, University of Dundee, Dundee, United Kingdom.
Brian R Bettencourt
Katsutomo Okamura
Tibor Csorba
Wibke Meyer
Zhigang Jin
Jason Biggerstaff
Haruhiko Siomi
Gyorgy Hutvagner
Eric C Lai
Michael Welte
H-Arno J Müller
University of Dundee · GBKettering University · USAlnylam Pharmaceuticals (United States) · USBoston University · USCell and Gene Therapy Catapult · GBHeinrich Heine University Düsseldorf · DEKeio University · JPNew York Audio Productions (United States) · USUniversity of Rochester · US

Funding

Selective regulatory and biogenesis mechanisms for microRNAsR01GM083300 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI Eric C Lai · 2007 to 2026
$9.8M
Developmental control of organelle transportR01GM064687 · NIGMS · UNIVERSITY OF ROCHESTER · PI WELTE, MICHAEL ANDREAS · 2002 to 2011
$2.2M
Medical Research Council G0501679Medical Research Council G0501679(76340)NIGMS NIH HHS GM64687NIGMS NIH HHS R01 GM064687NIGMS NIH HHS R01 GM083300NIGMS NIH HHS R01-GM083300Wellcome Trust
6 · The paper itself

Abstract

The Drosophila argonaute2 (ago2) gene plays a major role in siRNA mediated RNA silencing pathways. Unlike mammalian Argonaute proteins, the Drosophila protein has an unusual amino-terminal domain made up largely of multiple copies of glutamine-rich repeats (GRRs). We report here that the ago2 locus produces an alternative transcript that encodes a putative short isoform without this amino-terminal domain. Several ago2 mutations previously reported to be null alleles only abolish expression of the long, GRR-containing isoform. Analysis of drop out (dop) mutations had previously suggested that variations in GRR copy number result in defects in RNAi and embryonic development. However, we find that dop mutations genetically complement transcript-null alleles of ago2 and that ago2 alleles with variant GRR copy numbers support normal development. In addition, we show that the assembly of the central RNAi machinery, the RISC (RNA induced silencing complex), is unimpaired in embryos when GRR copy number is altered. In fact, we find that GRR copy number is highly variable in natural D. melanogaster populations as well as in laboratory strains. Finally, while many other insects share an extensive, glutamine-rich Ago2 amino-terminal domain, its primary sequence varies drastically between species. Our data indicate that GRR variation does not modulate an essential function of Ago2 and that the amino-terminal domain of Ago2 is subject to rapid evolution.

Indexed as

Gene Expression Regulation, DevelopmentalAllelesAnimalsArgonaute ProteinsDrosophila ProteinsFemaleGene DosageGene SilencingGenetic VariationGlutamineHeterozygoteMutationPhylogenyProtein IsoformsProtein Structure, TertiaryRNA-Induced Silencing ComplexAGO2 protein, DrosophilaArgonaute ProteinsDrosophila ProteinsGlutamineProtein IsoformsRNA-Induced Silencing Complex

Identifiers

PMID21253006
PMCPMC3002974
OpenAlexW2060303574

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.