Evidence map›Paper›PMID 26945040›Full record

ArticleNucleic acids research2016

Local potentiation of stress-responsive genes by upstream noncoding transcription.

Naomichi Takemata, Arisa Oda, Takatomi Yamada, Josephine Galipon, Tomoichiro Miyoshi, Yutaka Suzuki, Sumio Sugano, Charles S Hoffman, Kouji Hirota, Kunihiro Ohta

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

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  18. A current view on long noncoding RNAs in yeast and filamentous fungi.Applied microbiology and biotechnology · 2018
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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

10 authors at 5 institutions in 2 countries.

Naomichi TakemataDepartment of Life Sciences, The University of Tokyo, Meguro-ku, Tokyo 153-8902, Japan.
Arisa OdaDepartment of Life Sciences, The University of Tokyo, Meguro-ku, Tokyo 153-8902, Japan.
Takatomi YamadaDepartment of Biological Sciences, Chuo University, Bunkyo-ku, Tokyo 112-8551, Japan.
Josephine GaliponInstitute for Advanced Biosciences, Keio University, Tsuruoka, Yamagata 997-0035, Japan.
Tomoichiro MiyoshiDepartment of Life Sciences, The University of Tokyo, Meguro-ku, Tokyo 153-8902, Japan.
Yutaka SuzukiDepartment of Medical Genome Sciences, The University of Tokyo, Kashiwa, Chiba 277-8561, Japan.
Sumio SuganoDepartment of Medical Genome Sciences, The University of Tokyo, Kashiwa, Chiba 277-8561, Japan.
Charles S HoffmanBiology Department, Boston College, Chestnut Hill, MA 02467, USA.
Kouji HirotaDepartment of Chemistry, Tokyo Metropolitan University, Hachi-Ohji, Tokyo 192-0397, Japan.
Kunihiro OhtaDepartment of Life Sciences, The University of Tokyo, Meguro-ku, Tokyo 153-8902, Japan Department of Biological Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan kohta@bio.c.u-tokyo.ac.jp.
The University of Tokyo · JPBoston College · USChuo University · JPKeio University · JPTokyo Metropolitan University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been postulated that a myriad of long noncoding RNAs (lncRNAs) contribute to gene regulation. In fission yeast, glucose starvation triggers lncRNA transcription across promoter regions of stress-responsive genes including fbp1 (fructose-1,6-bisphosphatase1). At the fbp1 promoter, this transcription promotes chromatin remodeling and fbp1 mRNA expression. Here, we demonstrate that such upstream noncoding transcription facilitates promoter association of the stress-responsive transcriptional activator Atf1 at the sites of transcription, leading to activation of the downstream stress genes. Genome-wide analyses revealed that ∼50 Atf1-binding sites show marked decrease in Atf1 occupancy when cells are treated with a transcription inhibitor. Most of these transcription-enhanced Atf1-binding sites are associated with stress-dependent induction of the adjacent mRNAs or lncRNAs, as observed in fbp1 These Atf1-binding sites exhibit low Atf1 occupancy and high histone density in glucose-rich conditions, and undergo dramatic changes in chromatin status after glucose depletion: enhanced Atf1 binding, histone eviction, and histone H3 acetylation. We also found that upstream transcripts bind to the Groucho-Tup1 type transcriptional corepressors Tup11 and Tup12, and locally antagonize their repressive functions on Atf1 binding. These results reveal a new mechanism in which upstream noncoding transcription locally magnifies the specific activation of stress-inducible genes via counteraction of corepressors.

Indexed as

Gene Expression RegulationTranscription, GeneticAcetylationChromatin Assembly and DisassemblyChromatin ImmunoprecipitationGene Expression Regulation, FungalGlucoseHigh-Throughput Nucleotide SequencingHistonesProtein BindingRegulatory Sequences, Nucleic AcidRNA, UntranslatedSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsStress, PhysiologicalGlucoseHistonesRNA, UntranslatedSaccharomyces cerevisiae Proteins

Identifiers

PMID26945040
PMCPMC4914089
OpenAlexW2327906730

What OpenQuestion holds

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LicenceCC BY-NC
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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.