Evidence map›Paper›PMID 27540088›Full record

ArticleGenome research2016

Common genomic elements promote transcriptional and DNA replication roadblocks.

Kevin Roy, Jason Gabunilas, Abigail Gillespie, Duy Ngo, Guillaume F Chanfreau

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed, 41 citations in OpenAlex.

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  7. Splicing inactivation generates hybrid mRNA-snoRNA transcripts targeted by cytoplasmic RNA decay.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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

5 authors at 1 institution in 1 country.

Kevin RoyDepartment of Chemistry and Biochemistry, University of California, Los Angeles, Los Angeles, California 90095-1569, USA; Molecular Biology Institute, University of California, Los Angeles, Los Angeles, California 90095-1570, USA.
Jason GabunilasDepartment of Chemistry and Biochemistry, University of California, Los Angeles, Los Angeles, California 90095-1569, USA.
Abigail GillespieDepartment of Chemistry and Biochemistry, University of California, Los Angeles, Los Angeles, California 90095-1569, USA.
Duy NgoDepartment of Chemistry and Biochemistry, University of California, Los Angeles, Los Angeles, California 90095-1569, USA.
Guillaume F ChanfreauDepartment of Chemistry and Biochemistry, University of California, Los Angeles, Los Angeles, California 90095-1569, USA; Molecular Biology Institute, University of California, Los Angeles, Los Angeles, California 90095-1570, USA.ORCID 0000-0002-2505-1950
University of California, Los Angeles · US

Funding

UCLA NIGMS T32 Program AssessmentT32GM007185 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TORRES, JORGE · 1985 to 2020
$21.7M
THE CONTROL OF GENE EXPRESSION BY EUKARYOTIC RNASE IIIR01GM061518 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHANFREAU, GUILLAUME F · 2000 to 2017
$5.5M
NIGMS NIH HHS R01 GM061518NIGMS NIH HHS T32 GM007185
6 · The paper itself

Abstract

RNA polymerase II (Pol II) transcription termination by the Nrd1p-Nab3p-Sen1p (NNS) pathway is critical for the production of stable noncoding RNAs and the control of pervasive transcription in Saccharomyces cerevisiae To uncover determinants of NNS termination, we mapped the 3'-ends of NNS-terminated transcripts genome-wide. We found that nucleosomes and specific DNA-binding proteins, including the general regulatory factors (GRFs) Reb1p, Rap1p, and Abf1p, and Pol III transcription factors enhance the efficiency of NNS termination by physically blocking Pol II progression. The same DNA-bound factors that promote NNS termination were shown previously to define the 3'-ends of Okazaki fragments synthesized by Pol δ during DNA replication. Reduced binding of these factors results in defective NNS termination and Pol II readthrough. Furthermore, inactivating NNS enables Pol II elongation through these roadblocks, demonstrating that effective Pol II termination depends on a synergy between the NNS machinery and obstacles in chromatin. Consistent with this finding, loci exhibiting Pol II readthrough at GRF binding sites are depleted for upstream NNS signals. Overall, these results underscore how RNA termination signals influence the behavior of Pol II at chromatin obstacles, and establish that common genomic elements define boundaries for both DNA and RNA synthesis machineries.

Indexed as

DNA ReplicationGenome, FungalTranscription Elongation, GeneticTranscription Termination, GeneticDNADNA-Binding ProteinsDNA HelicasesDNA Polymerase IIDNA Polymerase IIINuclear ProteinsRNA-Binding ProteinsRNA HelicasesRNA, UntranslatedSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsShelterin ComplexABF1 protein, S cerevisiaeDNADNA-Binding ProteinsDNA HelicasesDNA Polymerase IIDNA Polymerase IIINAB3 protein, S cerevisiaeNRD1 protein, S cerevisiaeNuclear ProteinsOkazaki fragmentsRAP1 protein, S cerevisiaeREB1 protein, S cerevisiaeRNA-Binding ProteinsRNA HelicasesRNA, UntranslatedSaccharomyces cerevisiae ProteinsSEN1 protein, S cerevisiaeShelterin ComplexTelomere-Binding ProteinsTranscription Factors

Identifiers

PMID27540088
PMCPMC5052057
OpenAlexW2511759927

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.