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. 2020 May 7;11:2243. doi: 10.1038/s41467-020-16103-0

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — Generating a functional NSL complex interactome (represented as a blue network, left) enabled identification of BRD4 as the key interaction partner of the NSL complex in driving transcription of essential genes in Drosophila, mice and humans. Molecular characterization of this interaction led us to propose the following model (right): The NSL complex recruits BRD4 to target promoters via acetylation of the histone H4 tail, while BRD4 is required for the transition of RNA Pol2 from transcription initiation to elongation. Disturbance of the NSL complex–BRD4 axis by BET inhibitors (BETi) or KANSL1 haploinsufficiency (as seen in Koolen-de Vries syndrome) results in transcription elongation defects and compromised cellular homeostasis. BRD4 targeting defects can be restored by treatment with HDAC inhibitor (HDACi).