Evidence map›Paper›PMID 28811569›Full record

ArticleNature communications2017

Transcriptional response to stress is pre-wired by promoter and enhancer architecture.

Anniina Vihervaara, Dig Bijay Mahat, Michael J Guertin, Tinyi Chu, Charles G Danko, John T Lis, Lea Sistonen

Abstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing 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

96 citing papers in PubMed.

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36 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

7 authors.

Anniina VihervaaraFaculty of Science and Engineering, Cell Biology, Åbo Akademi University, Turku, 20520, Finland.
Dig Bijay MahatDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, New York, 14853, USA.
Michael J GuertinDepartment of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, Virginia, 22908, USA.
Tinyi ChuDepartment of Biomedical Sciences, The Baker Institute for Animal Health, Cornell University, Ithaca, New York, 14853, USA.
Charles G DankoDepartment of Biomedical Sciences, The Baker Institute for Animal Health, Cornell University, Ithaca, New York, 14853, USA.
John T LisDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, New York, 14853, USA. jtl10@cornell.edu.
Lea SistonenFaculty of Science and Engineering, Cell Biology, Åbo Akademi University, Turku, 20520, Finland. lea.sistonen@abo.fi.ORCID http://orcid.org/0000-0003-1341-2867

Funding

COORDINATE GENE REGULATION IN ANIMAL CELLSR01GM025232 · NIGMS · CORNELL UNIVERSITY ITHACA · PI LIS, JOHN T · 1985 to 2020
$8.4M
NIGMS NIH HHS R01 GM025232
6 · The paper itself

Abstract

Programs of gene expression are executed by a battery of transcription factors that coordinate divergent transcription from a pair of tightly linked core initiation regions of promoters and enhancers. Here, to investigate how divergent transcription is reprogrammed upon stress, we measured nascent RNA synthesis at nucleotide-resolution, and profiled histone H4 acetylation in human cells. Our results globally show that the release of promoter-proximal paused RNA polymerase into elongation functions as a critical switch at which a gene's response to stress is determined. Highly transcribed and highly inducible genes display strong transcriptional directionality and selective assembly of general transcription factors on the core sense promoter. Heat-induced transcription at enhancers, instead, correlates with prior binding of cell-type, sequence-specific transcription factors. Activated Heat Shock Factor 1 (HSF1) binds to transcription-primed promoters and enhancers, and CTCF-occupied, non-transcribed chromatin. These results reveal chromatin architectural features that orient transcription at divergent regulatory elements and prime transcriptional responses genome-wide.Heat Shock Factor 1 (HSF1) is a regulator of stress-induced transcription. Here, the authors investigate changes to transcription and chromatin organization upon stress and find that activated HSF1 binds to transcription-primed promoters and enhancers, and to CTCF occupied, untranscribed chromatin.

Indexed as

Enhancer Elements, GeneticGene Expression RegulationPromoter Regions, GeneticTranscription, GeneticAcetylationCell LineHeat-Shock ProteinsHeat-Shock ResponseHumansStress, PhysiologicalTranscription FactorsHeat-Shock ProteinsTranscription Factors

Identifiers

PMID28811569
PMCPMC5557961

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.