Evidence map›Paper›PMID 19850912›Full record

ArticleRNA (New York, N.Y.)2009

Nonsense-mediated mRNA decay mutes the splicing defects of spliceosome component mutations.

Tadashi Kawashima, Matteo Pellegrini, Guillaume F Chanfreau

Abstract read
In one paragraph

Article in RNA (New York, N.Y.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Splicing inactivation generates hybrid mRNA-snoRNA transcripts targeted by cytoplasmic RNA decay.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  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

3 authors.

Tadashi KawashimaDepartment of Chemistry and Biochemistry and the Molecular Biology Institute, University of California at Los Angeles, Los Angeles, California 90095-1569, USA.
Matteo Pellegrini
Guillaume F Chanfreau

Funding

THE CONTROL OF GENE EXPRESSION BY EUKARYOTIC RNASE IIIR01GM061518 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHANFREAU, GUILLAUME F · 2000 to 2017
$5.5M
PREDOCTORAL TRAINING PROGRAM IN GENETIC MECHANISMS AT UCT32GM007104 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GOBER, JAMES W · 1985 to 2011
$3.6M
NIGMS NIH HHS GM07104NIGMS NIH HHS GM61518NIGMS NIH HHS R01 GM061518NIGMS NIH HHS T32 GM007104
6 · The paper itself

Abstract

The role of many splicing factors in pre-mRNA splicing and the involvement of these factors in the processing of specific transcripts have often been defined through the analysis of loss-of-function mutants in vivo. Here we show that inactivating the nonsense-mediated mRNA decay (NMD) results in an enhancement of splicing phenotypes associated with several S. cerevisiae splicing factor mutations. Tiling microarrays showed that inactivation of the NMD factor Upf1p in the prp17Delta and prp18Delta mutant strains results in a larger spectrum of splicing defects than what is observed in the single mutants, including new transcripts previously shown unaffected by Prp17p or Prp18p inactivation. Inactivation of Upf1p in the second step/recycling factor prp22-1 mutant and in the nam8Delta and mud1Delta U1 snRNP component mutants also increase unspliced precursor accumulation of several specific transcripts. In addition, deletion of UPF1 partially suppresses the growth defects associated with the prp17Delta or prp22-1 mutations, demonstrating a positive genetic interaction between NMD and splicing factor mutants. These results show that RNA surveillance by NMD can mask some of the effects of splicing factor mutations, and that the roles of splicing factors cannot be fully understood in vivo unless RNA degradation systems that degrade unspliced precursors are also inactivated.

Indexed as

MutationRNA SplicingRNA StabilityCell Cycle ProteinsCodon, NonsenseDNA-Binding ProteinsRibonucleoprotein, U5 Small NuclearRNA-Binding ProteinsRNA HelicasesRNA Splicing FactorsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSpliceosomesTranscription, GeneticCDC40 protein, S cerevisiaeCell Cycle ProteinsCodon, NonsenseDNA-Binding ProteinsNAM7 protein, S cerevisiaePRP18 protein, S cerevisiaeRibonucleoprotein, U5 Small NuclearRNA-Binding ProteinsRNA HelicasesRNA Splicing FactorsSaccharomyces cerevisiae Proteins

Identifiers

PMID19850912
PMCPMC2779665

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.