Evidence map›Paper›PMID 26604986›Full record

ArticleEpigenetics & chromatin2015

CBP binding outside of promoters and enhancers in Drosophila melanogaster.

Philge Philip, Ann Boija, Roshan Vaid, Allison M Churcher, David J Meyers, Philip A Cole, Mattias Mannervik, Per Stenberg

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Epigenetics & chromatin, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

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  8. Polycomb-group recruitment to aScience advances · 2021
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  15. Sex combs reduced (Scr) regulatory region of Drosophila revisited.Molecular genetics and genomics : MGG · 2017
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 3 countries.

Philge PhilipDepartment of Molecular Biology, Umeå University, 901 87 Umeå, Sweden ; Computational Life Science Cluster (CLiC), Umeå University, 901 87 Umeå, Sweden ; Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad, Telangana 500007 India.
Ann BoijaDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 106 91 Stockholm, Sweden.
Roshan VaidDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 106 91 Stockholm, Sweden.
Allison M ChurcherDepartment of Molecular Biology, Umeå University, 901 87 Umeå, Sweden.
David J MeyersDepartment Pharmacology and Molecular Sciences, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205 USA.
Philip A ColeDepartment Pharmacology and Molecular Sciences, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205 USA.
Mattias MannervikDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 106 91 Stockholm, Sweden.
Per StenbergDepartment of Molecular Biology, Umeå University, 901 87 Umeå, Sweden ; Computational Life Science Cluster (CLiC), Umeå University, 901 87 Umeå, Sweden ; Division of CBRN Security and Defence, FOI-Swedish Defence Research Agency, Umeå, Sweden.
Stockholm University · SEJohns Hopkins Medicine · USCentre for Cellular and Molecular Biology · INSwedish Defence Research Agency · SEUmeå University · SE

Funding

Protein Acylation and Methylation Mechanisms_Administrative SupplementR37GM062437 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI COLE, PHILIP A · 2013 to 2022
$4.1M
NIGMS NIH HHS R37 GM062437
6 · The paper itself

Abstract

backgroundCREB-binding protein (CBP, also known as nejire) is a transcriptional co-activator that is conserved in metazoans. CBP plays an important role in embryonic development and cell differentiation and mutations in CBP can lead to various diseases in humans. In addition, CBP and the related p300 protein have successfully been used to predict enhancers in both humans and flies when they occur with monomethylation of histone H3 on lysine 4 (H3K4me1).

resultsHere, we compare CBP chromatin immunoprecipitation sequencing data from Drosophila S2 cells with modENCODE data and show that CBP is bound at genomic sites with a wide range of functions. As expected, we find that CBP is bound at active promoters and enhancers. In addition, we find that the strongest CBP sites in the genome are found at Polycomb response elements embedded in histone H3 lysine 27 trimethylated (H3K27me3) chromatin, where they correlate with binding of the Pho repressive complex. Interestingly, we find that CBP also binds to most insulators in the genome. At a subset of these, CBP may regulate insulating activity, measured as the ability to prevent repressive H3K27 methylation from spreading into adjacent chromatin.

conclusionsWe conclude that CBP could be involved in a much wider range of functions than has previously been appreciated, including Polycomb repression and insulator activity. In addition, we discuss the possibility that a common role for CBP at all functional elements may be to regulate interactions between distant chromosomal regions and speculate that CBP is controlling higher order chromatin organization.

Indexed as

CBP/p300Chromatin structureDrosophila melanogasterGene regulationInsulatorsPolycomb response elements

Identifiers

PMID26604986
PMCPMC4657240
OpenAlexW198005847

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.