Evidence map›Paper›PMID 29656924›Full record

ArticleMolecular cell2018

Cell-Cycle Modulation of Transcription Termination Factor Sen1.

Hannah E Mischo, Yujin Chun, Kevin M Harlen, Brendan M Smalec, Somdutta Dhir, L Stirling Churchman, Stephen Buratowski

Open access · hybridAbstract read
In one paragraph

Article in Molecular cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

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  7. Crosstalk of ubiquitin system and non-coding RNA in fibrosis.International journal of biological sciences · 2024
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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

7 authors at 3 institutions in 2 countries.

Hannah E MischoDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA; Sir William Dunn School of Pathology, Oxford University, South Parks Road, Oxford OX1 3RE, UK; Mechanisms of Transcription Laboratory, Clare Hall Laboratories, Cancer Research UK London Research Institute, South Mimms EN6 3LD, UK. Electronic address: hannah.mischo@path.ox.ac.uk.
Yujin ChunDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
Kevin M HarlenDepartment of Genetics, Harvard Medical School, Boston, MA 02115, USA.
Brendan M SmalecDepartment of Genetics, Harvard Medical School, Boston, MA 02115, USA.
Somdutta DhirSir William Dunn School of Pathology, Oxford University, South Parks Road, Oxford OX1 3RE, UK.
L Stirling ChurchmanDepartment of Genetics, Harvard Medical School, Boston, MA 02115, USA.
Stephen BuratowskiDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA. Electronic address: steveb@hms.harvard.edu.
Harvard University · USCancer Research UK · GBUniversity of Oxford · GB

Funding

The RNA Polymerase II Transcription CycleR01GM056663 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI Stephen Buratowski · 1999 to 2026
$11.7M
Mechanisms of Transcriptional Control Revealed by Nascent Transcript SequencingR01HG007173 · NHGRI · HARVARD MEDICAL SCHOOL · PI Lee Stirling Churchman · 2013 to 2026
$6.7M
Cancer Research UKNHGRI NIH HHS R01 HG007173NIGMS NIH HHS R01 GM056663Wellcome TrustWellcome Trust 089038/Z/09/ZWellcome Trust 091805/Z/10/Z
6 · The paper itself

Abstract

Many non-coding transcripts (ncRNA) generated by RNA polymerase II in S. cerevisiae are terminated by the Nrd1-Nab3-Sen1 complex. However, Sen1 helicase levels are surprisingly low compared with Nrd1 and Nab3, raising questions regarding how ncRNA can be terminated in an efficient and timely manner. We show that Sen1 levels increase during the S and G2 phases of the cell cycle, leading to increased termination activity of NNS. Overexpression of Sen1 or failure to modulate its abundance by ubiquitin-proteasome-mediated degradation greatly decreases cell fitness. Sen1 toxicity is suppressed by mutations in other termination factors, and NET-seq analysis shows that its overexpression leads to a decrease in ncRNA production and altered mRNA termination. We conclude that Sen1 levels are carefully regulated to prevent aberrant termination. We suggest that ncRNA levels and coding gene transcription termination are modulated by Sen1 to fulfill critical cell cycle-specific functions.

Indexed as

G1 Phase Cell Cycle CheckpointsGene Expression Regulation, FungalTranscription Termination, GeneticDNA HelicasesMicrobial ViabilityNuclear ProteinsProteasome Endopeptidase ComplexProteolysisRNA-Binding ProteinsRNA, FungalRNA HelicasesRNA, MessengerRNA, UntranslatedSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsUbiquitinationDNA HelicasesNAB3 protein, S cerevisiaeNRD1 protein, S cerevisiaeNuclear ProteinsProteasome Endopeptidase ComplexRNA-Binding ProteinsRNA, FungalRNA HelicasesRNA, MessengerRNA, UntranslatedSaccharomyces cerevisiae ProteinsSEN1 protein, S cerevisiaecell cycleNNSnon-coding RNANrd1-Nab3-Sen1Sen1transcription terminationubiquitin-proteasome system

Identifiers

PMID29656924
PMCPMC5919780
OpenAlexW2797299978

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.