Evidence map›Paper›PMID 31805520›Full record

ArticleGenes & development2020

A unified allosteric/torpedo mechanism for transcriptional termination on human protein-coding genes.

Joshua D Eaton, Laura Francis, Lee Davidson, Steven West

Abstract read
In one paragraph

Article in Genes & development, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing 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

81 citing papers in PubMed.

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  15. Toward structural understanding of eukaryotic transcription elongation.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2025
    Review
  16. Review
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21 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.

Joshua D EatonThe Living Systems Institute, University of Exeter, Exeter EX4 4QD, United Kingdom.
Laura FrancisThe Living Systems Institute, University of Exeter, Exeter EX4 4QD, United Kingdom.
Lee DavidsonThe Living Systems Institute, University of Exeter, Exeter EX4 4QD, United Kingdom.
Steven WestThe Living Systems Institute, University of Exeter, Exeter EX4 4QD, United Kingdom.

Funding

Biotechnology and Biological Sciences Research Council BB/K003240/1Medical Research Council MR/M008924/1Wellcome TrustWellcome Trust WT097835MFWellcome Trust WT101650MAWellcome Trust WT107791/Z/15/Z
6 · The paper itself

Abstract

The allosteric and torpedo models have been used for 30 yr to explain how transcription terminates on protein-coding genes. The former invokes termination via conformational changes in the transcription complex and the latter proposes that degradation of the downstream product of poly(A) signal (PAS) processing is important. Here, we describe a single mechanism incorporating features of both models. We show that termination is completely abolished by rapid elimination of CPSF73, which causes very extensive transcriptional readthrough genome-wide. This is because CPSF73 functions upstream of modifications to the elongation complex and provides an entry site for the XRN2 torpedo. Rapid depletion of XRN2 enriches these events that we show are underpinned by protein phosphatase 1 (PP1) activity, the inhibition of which extends readthrough in the absence of XRN2. Our results suggest a combined allosteric/torpedo mechanism, in which PP1-dependent slowing down of polymerases over termination regions facilitates their pursuit/capture by XRN2 following PAS processing.

Indexed as

Cell LineCleavage And Polyadenylation Specificity FactorExoribonucleasesGene DeletionHCT116 CellsHumansReceptors, Neuropeptide YRibonuclease HRNARNA Polymerase IITranscription Termination, GeneticCleavage And Polyadenylation Specificity FactorExoribonucleasesneuropeptide Y4 receptorReceptors, Neuropeptide YRibonuclease Hribonuclease HIRNARNA Polymerase IIXRN2 protein, humanantisense oligoCPSF73polyadenylation signalPP1RNA polymerase IItranscriptional terminationXRN2

Identifiers

PMID31805520
PMCPMC6938672

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Registered trials

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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.