Evidence map›Paper›PMID 26069324›Full record

ArticleThe EMBO journal2015

Chromatin signatures at Notch-regulated enhancers reveal large-scale changes in H3K56ac upon activation.

Lenka Skalska, Robert Stojnic, Jinghua Li, Bettina Fischer, Gustavo Cerda-Moya, Hiroshi Sakai, Shahragim Tajbakhsh, Steven Russell, Boris Adryan, Sarah J Bray

Abstract read
In one paragraph

Article in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing 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

50 citing papers in PubMed.

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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.

Lenka SkalskaDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.
Robert StojnicDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK Cambridge Systems Biology Centre, University of Cambridge, Cambridge, UK.
Jinghua LiDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.
Bettina FischerCambridge Systems Biology Centre, University of Cambridge, Cambridge, UK Department of Genetics, University of Cambridge, Cambridge, UK.
Gustavo Cerda-MoyaDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.
Hiroshi SakaiDepartment of Developmental & Stem Cell Biology, Institut Pasteur, Paris, France.
Shahragim TajbakhshDepartment of Developmental & Stem Cell Biology, Institut Pasteur, Paris, France.
Steven RussellCambridge Systems Biology Centre, University of Cambridge, Cambridge, UK Department of Genetics, University of Cambridge, Cambridge, UK.
Boris AdryanCambridge Systems Biology Centre, University of Cambridge, Cambridge, UK Department of Genetics, University of Cambridge, Cambridge, UK.
Sarah J BrayDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK sjb32@cam.ac.uk.

Funding

Biotechnology and Biological Sciences Research Council BB/J008842/1Medical Research Council G0800034Medical Research Council MR/L007177/1
6 · The paper itself

Abstract

The conserved Notch pathway functions in diverse developmental and disease-related processes, requiring mechanisms to ensure appropriate target selection and gene activation in each context. To investigate the influence of chromatin organisation and dynamics on the response to Notch signalling, we partitioned Drosophila chromatin using histone modifications and established the preferred chromatin conditions for binding of Su(H), the Notch pathway transcription factor. By manipulating activity of a co-operating factor, Lozenge/Runx, we showed that it can help facilitate these conditions. While many histone modifications were unchanged by Su(H) binding or Notch activation, we detected rapid changes in acetylation of H3K56 at Notch-regulated enhancers. This modification extended over large regions, required the histone acetyl-transferase CBP and was independent of transcription. Such rapid changes in H3K56 acetylation appear to be a conserved indicator of enhancer activation as they also occurred at the mammalian Notch-regulated Hey1 gene and at Drosophila ecdysone-regulated genes. This intriguing example of a core histone modification increasing over short timescales may therefore underpin changes in chromatin accessibility needed to promote transcription following signalling activation.

Indexed as

Enhancer Elements, GeneticAcetylationAnimalsCell Cycle ProteinsChromatinDNA-Binding ProteinsDNA, IntergenicDrosophila melanogasterDrosophila ProteinsEcdysoneGene Expression RegulationHistone AcetyltransferasesHistonesp300-CBP Transcription FactorsReceptors, NotchRepressor ProteinsCell Cycle ProteinsChromatinDNA-Binding ProteinsDNA, IntergenicDrosophila ProteinsEcdysoneHey1 protein, mouseHistone AcetyltransferasesHistoneslz protein, Drosophilanej protein, DrosophilaN protein, Drosophilap300-CBP Transcription FactorsReceptors, NotchRepressor ProteinsSu(H) protein, DrosophilaTranscription FactorsCBP/Nejirechromatin stateCSLH3K56acNotch

Identifiers

PMID26069324
PMCPMC4547894

What OpenQuestion holds

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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.