Evidence map›Paper›PMID 31522989›Full record

ArticleMolecular cell2019

A Complex of U1 snRNP with Cleavage and Polyadenylation Factors Controls Telescripting, Regulating mRNA Transcription in Human Cells.

Byung Ran So, Chao Di, Zhiqiang Cai, Christopher C Venters, Jiannan Guo, Jung-Min Oh, Chie Arai, Gideon Dreyfuss

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

66 citing papers in PubMed, 116 citations in OpenAlex.

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6 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

8 authors at 2 institutions in 1 country.

Byung Ran SoHoward Hughes Medical Institute, Department of Biochemistry and Biophysics, University of Pennsylvania, School of Medicine, Philadelphia, PA 19104, USA.
Chao DiHoward Hughes Medical Institute, Department of Biochemistry and Biophysics, University of Pennsylvania, School of Medicine, Philadelphia, PA 19104, USA.
Zhiqiang CaiHoward Hughes Medical Institute, Department of Biochemistry and Biophysics, University of Pennsylvania, School of Medicine, Philadelphia, PA 19104, USA.
Christopher C VentersHoward Hughes Medical Institute, Department of Biochemistry and Biophysics, University of Pennsylvania, School of Medicine, Philadelphia, PA 19104, USA.
Jiannan GuoHoward Hughes Medical Institute, Department of Biochemistry and Biophysics, University of Pennsylvania, School of Medicine, Philadelphia, PA 19104, USA.
Jung-Min OhHoward Hughes Medical Institute, Department of Biochemistry and Biophysics, University of Pennsylvania, School of Medicine, Philadelphia, PA 19104, USA.
Chie AraiHoward Hughes Medical Institute, Department of Biochemistry and Biophysics, University of Pennsylvania, School of Medicine, Philadelphia, PA 19104, USA.
Gideon DreyfussHoward Hughes Medical Institute, Department of Biochemistry and Biophysics, University of Pennsylvania, School of Medicine, Philadelphia, PA 19104, USA. Electronic address: gdreyfuss@hhmi.upenn.edu.
University of Pennsylvania · USHoward Hughes Medical Institute · US

Funding

Mechanism of U1 snRNPs suppression of premature cleavage & polyadenylationR01GM112923 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI DREYFUSS, GIDEON · 2015 to 2018
$1.6M
Howard Hughes Medical InstituteNIGMS NIH HHS R01 GM112923
6 · The paper itself

Abstract

Full-length transcription in the majority of human genes depends on U1 snRNP (U1) to co-transcriptionally suppress transcription-terminating premature 3' end cleavage and polyadenylation (PCPA) from cryptic polyadenylation signals (PASs) in introns. However, the mechanism of this U1 activity, termed telescripting, is unknown. Here, we captured a complex, comprising U1 and CPA factors (U1-CPAFs), that binds intronic PASs and suppresses PCPA. U1-CPAFs are distinct from U1-spliceosomal complexes; they include CPA's three main subunits, CFIm, CPSF, and CstF; lack essential splicing factors; and associate with transcription elongation and mRNA export complexes. Telescripting requires U1:pre-mRNA base-pairing, which can be disrupted by U1 antisense oligonucleotide (U1 AMO), triggering PCPA. U1 AMO remodels U1-CPAFs, revealing changes, including recruitment of CPA-stimulating factors, that explain U1-CPAFs' switch from repressive to activated states. Our findings outline this U1 telescripting mechanism and demonstrate U1's unique role as central regulator of pre-mRNA processing and transcription.

Indexed as

RNA CleavageTranscription, Genetic3' Untranslated RegionsActive Transport, Cell NucleusBinding SitesCell NucleusCleavage And Polyadenylation Specificity FactorCleavage Stimulation FactorHeLa CellsHumansMultiprotein ComplexesPoly AProtein BindingRibonucleoprotein, U1 Small NuclearRNA, MessengerRNA Precursors3' Untranslated RegionsCleavage And Polyadenylation Specificity FactorCleavage Stimulation FactorMultiprotein ComplexesPoly ARibonucleoprotein, U1 Small NuclearRNA, MessengerRNA Precursorscleavage and polyadenylation-end processingmRNA 3ʹtelescriptingtranscription elongationtranscription terminationU1 snRNP

Identifiers

PMID31522989
PMCPMC6874754
OpenAlexW2972807540

What OpenQuestion holds

Textmetadata
LicenceTDM
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.