Evidence map›Paper›PMID 34172724›Full record

ArticleNature communications2021

SMG5-SMG7 authorize nonsense-mediated mRNA decay by enabling SMG6 endonucleolytic activity.

Volker Boehm, Sabrina Kueckelmann, Jennifer V Gerbracht, Sebastian Kallabis, Thiago Britto-Borges, Janine Altmüller, Marcus Krüger, Christoph Dieterich, Niels H Gehring

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
6.0field-weighted citation impact, top 2% 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

64 citing papers in PubMed, 101 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
  6. Nonsense-mediated mRNA decay: friend or foe in cancer biology?Cell communication and signaling : CCS · 2026
    Review
  7. Review
  8. NMD takes two PIN domains to tango.RNA (New York, N.Y.) · 2026
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

4 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 at 3 institutions in 1 country.

Volker Boehm *Institute for Genetics, University of Cologne, Cologne, Germany. boehmv@uni-koeln.de.ORCID 0000-0001-7588-9842
Sabrina Kueckelmann *Institute for Genetics, University of Cologne, Cologne, Germany.ORCID 0000-0001-8070-8823
Jennifer V GerbrachtInstitute for Genetics, University of Cologne, Cologne, Germany.
Sebastian KallabisCECAD Research Center, University of Cologne, Cologne, Germany.
Thiago Britto-BorgesSection of Bioinformatics and Systems Cardiology, Department of Internal Medicine III and Klaus Tschira Institute for Integrative Computational Cardiology, Heidelberg University Hospital, Heidelberg, Germany.ORCID 0000-0002-6218-4429
Janine AltmüllerCologne Center for Genomics (CCG), University of Cologne, Cologne, Germany.
Marcus KrügerCenter for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.ORCID 0000-0002-5846-6941
Christoph DieterichSection of Bioinformatics and Systems Cardiology, Department of Internal Medicine III and Klaus Tschira Institute for Integrative Computational Cardiology, Heidelberg University Hospital, Heidelberg, Germany.
Niels H GehringInstitute for Genetics, University of Cologne, Cologne, Germany. ngehring@uni-koeln.de.ORCID 0000-0001-7792-1164
University of Cologne · DEHeidelberg University · DETH Köln - University of Applied Sciences · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Eukaryotic gene expression is constantly controlled by the translation-coupled nonsense-mediated mRNA decay (NMD) pathway. Aberrant translation termination leads to NMD activation, resulting in phosphorylation of the central NMD factor UPF1 and robust clearance of NMD targets via two seemingly independent and redundant mRNA degradation branches. Here, we uncover that the loss of the first SMG5-SMG7-dependent pathway also inactivates the second SMG6-dependent branch, indicating an unexpected functional connection between the final NMD steps. Transcriptome-wide analyses of SMG5-SMG7-depleted cells confirm exhaustive NMD inhibition resulting in massive transcriptomic alterations. Intriguingly, we find that the functionally underestimated SMG5 can substitute the role of SMG7 and individually activate NMD. Furthermore, the presence of either SMG5 or SMG7 is sufficient to support SMG6-mediated endonucleolysis of NMD targets. Our data support an improved model for NMD execution that features two-factor authentication involving UPF1 phosphorylation and SMG5-SMG7 recruitment to access SMG6 activity.

Indexed as

Carrier ProteinsCell LineEndoribonucleasesFemaleGene Knockout TechniquesHumansNonsense Mediated mRNA DecayPhosphorylationRNA HelicasesTelomeraseTrans-ActivatorsCarrier ProteinsEndoribonucleasesRNA HelicasesSMG5 protein, humanSMG6 protein, humanSMG7 protein, humanTelomeraseTrans-ActivatorsUPF1 protein, human

Identifiers

PMID34172724
PMCPMC8233366
OpenAlexW3177373917

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.