Evidence map›Paper›PMID 32382029›Full record

ArticleNature communications2020

Evolutionary conserved NSL complex/BRD4 axis controls transcription activation via histone acetylation.

Aline Gaub, Bilal N Sheikh, M Felicia Basilicata, Marie Vincent, Mathilde Nizon, Cindy Colson, Matthew J Bird, James E Bradner, Julien Thevenon, Michael Boutros and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. 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
1.7field-weighted citation impact, top 16% 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, 41 citations in OpenAlex.

  1. Review
  2. Article
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  7. Non-Classic Cornelia de Lange Syndrome Due toChildren (Basel, Switzerland) · 2025
    Review
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  9. Article
  10. Acetyltransferase in cardiovascular disease and aging.The journal of cardiovascular aging · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
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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

11 authors at 6 institutions in 3 countries.

Aline GaubMax Planck Institute of Immunobiology and Epigenetics, Stuebeweg 51, 79108, Freiburg, Germany.ORCID http://orcid.org/0000-0002-3571-9547
Bilal N SheikhMax Planck Institute of Immunobiology and Epigenetics, Stuebeweg 51, 79108, Freiburg, Germany.ORCID http://orcid.org/0000-0002-1970-6236
M Felicia BasilicataMax Planck Institute of Immunobiology and Epigenetics, Stuebeweg 51, 79108, Freiburg, Germany.ORCID http://orcid.org/0000-0002-1111-9459
Marie VincentCHU Nantes, Service de Génétique Médicale, 38 Boulevard Jean Monnet, 44000, Nantes, France.ORCID http://orcid.org/0000-0003-1010-5618
Mathilde NizonCHU Nantes, Service de Génétique Médicale, 38 Boulevard Jean Monnet, 44000, Nantes, France.
Cindy ColsonService Génétique, Génétique Clinique, CHU, Avenue Georges Clemenceau CS 30001, 14033, Caen, France.
Matthew J BirdDepartment of Chronic Diseases, Metabolism and Ageing, Katholieke Universiteit Leuven, Herestraat 49, 3000, Leuven, Belgium.
James E BradnerNovartis Institutes for Biomedical Research, 181 Massachusetts Ave, Cambridge, MA, 02139, USA.ORCID http://orcid.org/0000-0002-2718-4415
Julien ThevenonCNRS UMR 5309, INSERM, U1209, Institute of Advanced Biosciences, Université Grenoble-Alpes CHU Grenoble, Allée des Alpes, 38700, La Tronche Grenoble, France.
Michael BoutrosDivision of Signaling and Functional Genomics, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 580, 69120, Heidelberg, Germany.
Asifa AkhtarMax Planck Institute of Immunobiology and Epigenetics, Stuebeweg 51, 79108, Freiburg, Germany. akhtar@ie-freiburg.mpg.de.ORCID http://orcid.org/0000-0001-8973-6193
Max Planck Institute of Immunobiology and Epigenetics · DEGénétique Médicale & Génomique Fonctionelle · FRCentre National de la Recherche Scientifique · FRGerman Cancer Research Center · DEKU Leuven · BEUniversité de Caen Normandie · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cells rely on a diverse repertoire of genes for maintaining homeostasis, but the transcriptional networks underlying their expression remain poorly understood. The MOF acetyltransferase-containing Non-Specific Lethal (NSL) complex is a broad transcription regulator. It is essential in Drosophila, and haploinsufficiency of the human KANSL1 subunit results in the Koolen-de Vries syndrome. Here, we perform a genome-wide RNAi screen and identify the BET protein BRD4 as an evolutionary conserved co-factor of the NSL complex. Using Drosophila and mouse embryonic stem cells, we characterise a recruitment hierarchy, where NSL-deposited histone acetylation enables BRD4 recruitment for transcription of constitutively active genes. Transcriptome analyses in Koolen-de Vries patient-derived fibroblasts reveals perturbations with a cellular homeostasis signature that are evoked by the NSL complex/BRD4 axis. We propose that BRD4 represents a conserved bridge between the NSL complex and transcription activation, and provide a new perspective in the understanding of their functions in healthy and diseased states.

Indexed as

AcetylationAnimalsCells, CulturedChromatinDrosophilaDrosophila ProteinsEpigenomicsFemaleGene Expression ProfilingHistonesMaleMiceNuclear ProteinsPregnancyPromoter Regions, GeneticRNA InterferenceChromatinDrosophila ProteinsHistonesNuclear Proteins

Identifiers

PMID32382029
PMCPMC7206058
OpenAlexW3023788214

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.