Evidence map›Paper›PMID 30819644›Full record

ArticleMolecular cell2019

Selective Roles of Vertebrate PCF11 in Premature and Full-Length Transcript Termination.

Kinga Kamieniarz-Gdula, Michal R Gdula, Karin Panser, Takayuki Nojima, Joan Monks, Jacek R Wiśniewski, Joey Riepsaame, Neil Brockdorff, Andrea Pauli, Nick J Proudfoot

Open access · hybridAbstract 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 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
6.9field-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

92 citing papers in PubMed, 150 citations in OpenAlex.

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32 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

10 authors at 3 institutions in 3 countries.

Kinga Kamieniarz-GdulaSir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK. Electronic address: kinga.kamieniarz-gdula@path.ox.ac.uk.
Michal R GdulaDepartment of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK.
Karin PanserResearch Institute of Molecular Pathology (IMP), Vienna Biocenter (VBC), Campus-Vienna-Biocenter 1, 1030 Vienna, Austria.
Takayuki NojimaSir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK.
Joan MonksSir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK.
Jacek R WiśniewskiBiochemical Proteomics Group, Department of Proteomics and Signal Transduction, Max-Planck Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany.
Joey RiepsaameSir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK.
Neil BrockdorffDepartment of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK.
Andrea PauliResearch Institute of Molecular Pathology (IMP), Vienna Biocenter (VBC), Campus-Vienna-Biocenter 1, 1030 Vienna, Austria. Electronic address: andrea.pauli@imp.ac.at.
Nick J ProudfootSir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK. Electronic address: nicholas.proudfoot@path.ox.ac.uk.
University of Oxford · GBResearch Institute of Molecular Pathology · ATMax Planck Institute of Biochemistry · DE

Funding

Wellcome Trust 103768
6 · The paper itself

Abstract

The pervasive nature of RNA polymerase II (Pol II) transcription requires efficient termination. A key player in this process is the cleavage and polyadenylation (CPA) factor PCF11, which directly binds to the Pol II C-terminal domain and dismantles elongating Pol II from DNA in vitro. We demonstrate that PCF11-mediated termination is essential for vertebrate development. A range of genomic analyses, including mNET-seq, 3' mRNA-seq, chromatin RNA-seq, and ChIP-seq, reveals that PCF11 enhances transcription termination and stimulates early polyadenylation genome-wide. PCF11 binds preferentially between closely spaced genes, where it prevents transcriptional interference and consequent gene downregulation. Notably, PCF11 is sub-stoichiometric to the CPA complex. Low levels of PCF11 are maintained by an auto-regulatory mechanism involving premature termination of its own transcript and are important for normal development. Both in human cell culture and during zebrafish development, PCF11 selectively attenuates the expression of other transcriptional regulators by premature CPA and termination.

Indexed as

Transcription Termination, GeneticAnimalsAnimals, Genetically ModifiedBinding SitesGene Expression Regulation, DevelopmentalHeLa CellsHumansmRNA Cleavage and Polyadenylation FactorsMutationPolyadenylationProtein BindingRNA CleavageRNA, MessengerRNA Polymerase IIZebrafishZebrafish ProteinsmRNA Cleavage and Polyadenylation FactorsPcf11 protein, humanpcf11 protein, zebrafishRNA, MessengerRNA Polymerase IIZebrafish Proteinsalternative polyadenylationattenuationautoregulationhumanPCF11premature terminationregulation of gene expressionRNA 3′ processingtranscription terminationzebrafish

Identifiers

PMID30819644
PMCPMC6458999
OpenAlexW2904191166

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.