Evidence map›Paper›PMID 25147240›Full record

ArticleRNA (New York, N.Y.)2014

The interaction of cytoplasmic poly(A)-binding protein with eukaryotic initiation factor 4G suppresses nonsense-mediated mRNA decay.

Tobias Fatscher, Volker Boehm, Benjamin Weiche, Niels H Gehring

Open access · bronzeAbstract read
In one paragraph

Article in RNA (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

  1. Pooled it
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  15. Cell cycle (Georgetown, Tex.) · 2023
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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

4 authors at 2 institutions in 1 country.

Tobias FatscherInstitute for Genetics, University of Cologne, 50674 Cologne, Germany.
Volker BoehmInstitute for Genetics, University of Cologne, 50674 Cologne, Germany.
Benjamin WeicheInstitute for Genetics, University of Cologne, 50674 Cologne, Germany.
Niels H GehringInstitute for Genetics, University of Cologne, 50674 Cologne, Germany ngehring@uni-koeln.de.
University of Cologne · DETH Köln - University of Applied Sciences · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonsense-mediated mRNA decay (NMD) eliminates different classes of mRNA substrates including transcripts with long 3' UTRs. Current models of NMD suggest that the long physical distance between the poly(A) tail and the termination codon reduces the interaction between cytoplasmic poly(A)-binding protein (PABPC1) and the eukaryotic release factor 3a (eRF3a) during translation termination. In the absence of PABPC1 binding, eRF3a recruits the NMD factor UPF1 to the terminating ribosome, triggering mRNA degradation. Here, we have used the MS2 tethering system to investigate the suppression of NMD by PABPC1. We show that tethering of PABPC1 between the termination codon and a long 3' UTR specifically inhibits NMD-mediated mRNA degradation. Contrary to the current model, tethered PABPC1 mutants unable to interact with eRF3a still efficiently suppress NMD. We find that the interaction of PABPC1 with eukaryotic initiation factor 4G (eIF4G), which mediates the circularization of mRNAs, is essential for NMD inhibition by tethered PABPC1. Furthermore, recruiting either eRF3a or eIF4G in proximity to an upstream termination codon antagonizes NMD. While tethering of an eRF3a mutant unable to interact with PABPC1 fails to suppress NMD, tethered eIF4G inhibits NMD in a PABPC1-independent manner, indicating a sequential arrangement of NMD antagonizing factors. In conclusion, our results establish a previously unrecognized link between translation termination, mRNA circularization, and NMD suppression, thereby suggesting a revised model for the activation of NMD at termination codons upstream of long 3' UTR.

Indexed as

Blotting, NorthernCodon, NonsenseCytoplasmEukaryotic Initiation Factor-4GHeLa CellsHumansImmunoblottingImmunoprecipitationNonsense Mediated mRNA DecayPeptide Termination FactorsPoly APoly(A)-Binding Protein IProtein BiosynthesisRibosomesRNA, MessengerCodon, NonsenseEIF4G1 protein, humanEukaryotic Initiation Factor-4Gpeptide-chain-release factor 3Peptide Termination FactorsPoly APoly(A)-Binding Protein IRNA, MessengereIF4GNMDPABPC1ribosome recyclingtranslation termination

Identifiers

PMID25147240
PMCPMC4174440
OpenAlexW2163899058

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.