Evidence map›Paper›PMID 25252976›Full record

ArticleNature2014

Regulation of RNA polymerase II activation by histone acetylation in single living cells.

Timothy J Stasevich, Yoko Hayashi-Takanaka, Yuko Sato, Kazumitsu Maehara, Yasuyuki Ohkawa, Kumiko Sakata-Sogawa, Makio Tokunaga, Takahiro Nagase, Naohito Nozaki, James G McNally and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 184 papers.

0numbers the graph read from it
0cells of the map it votes in
184citing papers in PubMed
14.8field-weighted citation impact, top 1% 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

184 citing papers in PubMed, 311 citations in OpenAlex.

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124 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

11 authors at 6 institutions in 2 countries.

Timothy J Stasevich1] Graduate School of Frontier Biosciences, Osaka University, Osaka, 565-0871, Japan [2] Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, Colorado 80523-1870, USA [3] Transcription Imaging Consortium, Janelia Farm Research Campus, Howard Hughes Medical Institute, Ashburn, Virginia 20147, USA.
Yoko Hayashi-Takanaka1] Graduate School of Frontier Biosciences, Osaka University, Osaka, 565-0871, Japan [2] Japan Science and Technology Agency (JST), Core Research for Evolutional Science and Technology (CREST), Kawaguchi, Saitama, 332-0012, Japan [3] Department of Biological Sciences, Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, Yokohama, 226-8501, Japan.
Yuko Sato1] Graduate School of Frontier Biosciences, Osaka University, Osaka, 565-0871, Japan [2] Department of Biological Sciences, Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, Yokohama, 226-8501, Japan.
Kazumitsu MaeharaDepartment of Advanced Medical Initiatives, Faculty of Medicine, Kyushu University, Fukuoka, 812-8582, Japan.
Yasuyuki Ohkawa1] Japan Science and Technology Agency (JST), Core Research for Evolutional Science and Technology (CREST), Kawaguchi, Saitama, 332-0012, Japan [2] Department of Advanced Medical Initiatives, Faculty of Medicine, Kyushu University, Fukuoka, 812-8582, Japan.
Kumiko Sakata-Sogawa1] Department of Biological Information, Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, Yokohama, 226-8501, Japan [2] RIKEN Center for Integrative Medical Sciences (IMS), Yokohama, 230-0045, Japan.
Makio Tokunaga1] Department of Biological Information, Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, Yokohama, 226-8501, Japan [2] RIKEN Center for Integrative Medical Sciences (IMS), Yokohama, 230-0045, Japan.
Takahiro NagaseDepartment of Biotechnology Research, Kazusa DNA Research Institute, Chiba, 292-0818, Japan.
Naohito NozakiMab Institute Inc., Sapporo, 001-0021, Japan.
James G McNally1] Laboratory of Receptor Biology and Gene Expression, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA [2] Institute for Soft Matter and Functional Materials, Helmholtz Zentrum Berlin, Berlin, 14109, Germany.
Hiroshi Kimura1] Graduate School of Frontier Biosciences, Osaka University, Osaka, 565-0871, Japan [2] Japan Science and Technology Agency (JST), Core Research for Evolutional Science and Technology (CREST), Kawaguchi, Saitama, 332-0012, Japan [3] Department of Biological Sciences, Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, Yokohama, 226-8501, Japan.
Osaka University · JPTokyo Institute of Technology · JPJapan Science and Technology Agency · JPKazusa DNA Research Institute · JPKyushu University · JPNational Institutes of Health · US

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

In eukaryotic cells, post-translational histone modifications have an important role in gene regulation. Starting with early work on histone acetylation, a variety of residue-specific modifications have now been linked to RNA polymerase II (RNAP2) activity, but it remains unclear if these markers are active regulators of transcription or just passive byproducts. This is because studies have traditionally relied on fixed cell populations, meaning temporal resolution is limited to minutes at best, and correlated factors may not actually be present in the same cell at the same time. Complementary approaches are therefore needed to probe the dynamic interplay of histone modifications and RNAP2 with higher temporal resolution in single living cells. Here we address this problem by developing a system to track residue-specific histone modifications and RNAP2 phosphorylation in living cells by fluorescence microscopy. This increases temporal resolution to the tens-of-seconds range. Our single-cell analysis reveals histone H3 lysine-27 acetylation at a gene locus can alter downstream transcription kinetics by as much as 50%, affecting two temporally separate events. First acetylation enhances the search kinetics of transcriptional activators, and later the acetylation accelerates the transition of RNAP2 from initiation to elongation. Signatures of the latter can be found genome-wide using chromatin immunoprecipitation followed by sequencing. We argue that this regulation leads to a robust and potentially tunable transcriptional response.

Indexed as

Single-Cell AnalysisTranscription, GeneticAcetylationAnimalsCell Line, TumorCell SurvivalChromatin ImmunoprecipitationEnzyme ActivationGenomeHistonesKineticsLysineMiceMicroscopy, FluorescencePhosphorylationRNA Polymerase IIHistonesLysineRNA Polymerase II

Identifiers

PMID25252976
OpenAlexW2010259456

What OpenQuestion holds

Textmetadata
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.