Evidence map›Paper›PMID 19487564›Full record

ArticleGenetics2009

Genetic modifiers of dFMR1 encode RNA granule components in Drosophila.

Anne-Marie J Cziko, Cathal T McCann, Iris C Howlett, Scott A Barbee, Rebecca P Duncan, Rene Luedemann, Daniela Zarnescu, Konrad E Zinsmaier, Roy R Parker, Mani Ramaswami

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Frontiers in genetics · 2019
    Review
  6. Modeling Fragile X Syndrome inFrontiers in molecular neuroscience · 2018
    Review
  7. Article
  8. dFmr1 Plays Roles in Small RNA Pathways of Drosophila melanogaster.International journal of molecular sciences · 2017
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. FMRP and Ataxin-2 function together in long-term olfactory habituation and neuronal translational control.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  17. RNA-binding protein misregulation in microsatellite expansion disorders.Advances in experimental medicine and biology · 2014
    Review
  18. Article
  19. Article
  20. 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

10 authors at 2 institutions in 2 countries.

Anne-Marie J CzikoSmurfit Institute of Genetics and Trinity College Institute for Neuroscience, Trinity College Dublin, Dublin-2, Ireland.
Cathal T McCann
Iris C Howlett
Scott A Barbee
Rebecca P Duncan
Rene Luedemann
Daniela Zarnescu
Konrad E Zinsmaier
Roy R Parker
Mani Ramaswami
Trinity College Dublin · IEUniversity of Arizona · US

Funding

P-Body and miRNA-Mediated Regulation of NeuroplasticityR01DA026048 · NIDA · UNIVERSITY OF DENVER (COLORADO SEMINARY) · PI BARBEE, SCOTT A · 2008 to 2011
$1.2M
Translational Regulation of Synaptic PlasticityF31NS055479 · NINDS · UNIVERSITY OF ARIZONA · PI CZIKO, ANNE-MARIE J · 2006 to 2007
$67k
NIDA NIH HHS R01 DA026048NINDS NIH HHS F31 NS055479NINDS NIH HHS F31 NS055479-01
6 · The paper itself

Abstract

Mechanisms of neuronal mRNA localization and translation are of considerable biological interest. Spatially regulated mRNA translation contributes to cell-fate decisions and axon guidance during development, as well as to long-term synaptic plasticity in adulthood. The Fragile-X Mental Retardation protein (FMRP/dFMR1) is one of the best-studied neuronal translational control molecules and here we describe the identification and early characterization of proteins likely to function in the dFMR1 pathway. Induction of the dFMR1 in sevenless-expressing cells of the Drosophila eye causes a disorganized (rough) eye through a mechanism that requires residues necessary for dFMR1/FMRP's translational repressor function. Several mutations in dco, orb2, pAbp, rm62, and smD3 genes dominantly suppress the sev-dfmr1 rough-eye phenotype, suggesting that they are required for dFMR1-mediated processes. The encoded proteins localize to dFMR1-containing neuronal mRNPs in neurites of cultured neurons, and/or have an effect on dendritic branching predicted for bona fide neuronal translational repressors. Genetic mosaic analyses indicate that dco, orb2, rm62, smD3, and dfmr1 are dispensable for translational repression of hid, a microRNA target gene, known to be repressed in wing discs by the bantam miRNA. Thus, the encoded proteins may function as miRNA- and/or mRNA-specific translational regulators in vivo.

Indexed as

AllelesAnimalsBiological TransportCells, CulturedDrosophilaDrosophila ProteinsEyeFragile X Messenger Ribonucleoprotein 1MicroRNAsMutationNeuronsRibonucleoproteinsRNA, MessengerDrosophila ProteinsFMR1 protein, DrosophilaFragile X Messenger Ribonucleoprotein 1messenger ribonucleoproteinMicroRNAsRibonucleoproteinsRNA, Messenger

Identifiers

PMID19487564
PMCPMC2728847
OpenAlexW2135105795

What OpenQuestion holds

Textmetadata
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.