Evolutionary conserved NSL complex/BRD4 axis controls transcription activation via histone acetylation
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, an...
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| Hauptverfasser: | , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
May 7, 2020
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| In: |
Nature Communications
Year: 2020, Jahrgang: 11 |
| ISSN: | 2041-1723 |
| DOI: | 10.1038/s41467-020-16103-0 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1038/s41467-020-16103-0 Verlag, lizenzpflichtig, Volltext: https://www.nature.com/articles/s41467-020-16103-0 
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| Verfasserangaben: | Aline Gaub, Bilal N. Sheikh, M. Felicia Basilicata, Marie Vincent, Mathilde Nizon, Cindy Colson, Matthew J. Bird, James E. Bradner, Julien Thevenon, Michael Boutros & Asifa Akhtar |
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| 520 | |a 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. | ||
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| 700 | 1 | |a Basilicata, M. Felicia |e VerfasserIn |4 aut | |
| 700 | 1 | |a Vincent, Marie |e VerfasserIn |4 aut | |
| 700 | 1 | |a Nizon, Mathilde |e VerfasserIn |4 aut | |
| 700 | 1 | |a Colson, Cindy |e VerfasserIn |4 aut | |
| 700 | 1 | |a Bird, Matthew J. |e VerfasserIn |4 aut | |
| 700 | 1 | |a Bradner, James E. |e VerfasserIn |4 aut | |
| 700 | 1 | |a Thevenon, Julien |e VerfasserIn |4 aut | |
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| 700 | 1 | |a Akhtar, Asifa |e VerfasserIn |4 aut | |
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