EcR recruits dMi-2 and increases efficiency of dMi-2-mediated remodelling to constrain transcription of hormone-regulated genes

Judith Kreher, Kristina Kovač, Karim Bouazoune, Igor Mačinković, Anna Luise Ernst, Erik Engelen, Roman Pahl, Florian Finkernagel, Magdalena Murawska, Ikram Ullah and Alexander Brehm ()
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Judith Kreher: Institute of Molecular Biology and Tumour Research, Philipps University Marburg
Kristina Kovač: Institute of Molecular Biology and Tumour Research, Philipps University Marburg
Karim Bouazoune: Institute of Molecular Biology and Tumour Research, Philipps University Marburg
Igor Mačinković: Institute of Molecular Biology and Tumour Research, Philipps University Marburg
Anna Luise Ernst: Institute of Molecular Biology and Tumour Research, Philipps University Marburg
Erik Engelen: Institute of Molecular Biology and Tumour Research, Philipps University Marburg
Roman Pahl: Institute of Medical Biometry and Epidemiology, Philipps University Marburg
Florian Finkernagel: Center for Tumour Biology and Immunology, Philipps University Marburg
Magdalena Murawska: Institute of Molecular Biology and Tumour Research, Philipps University Marburg
Ikram Ullah: Institute of Molecular Biology and Tumour Research, Philipps University Marburg
Alexander Brehm: Institute of Molecular Biology and Tumour Research, Philipps University Marburg

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract Gene regulation by steroid hormones plays important roles in health and disease. In Drosophila, the hormone ecdysone governs transitions between key developmental stages. Ecdysone-regulated genes are bound by a heterodimer of ecdysone receptor (EcR) and Ultraspiracle. According to the bimodal switch model, steroid hormone receptors recruit corepressors in the absence of hormone and coactivators in its presence. Here we show that the nucleosome remodeller dMi-2 is recruited to ecdysone-regulated genes to limit transcription. Contrary to the prevalent model, recruitment of the dMi-2 corepressor increases upon hormone addition to constrain gene activation through chromatin remodelling. Furthermore, EcR and dMi-2 form a complex that is devoid of Ultraspiracle. Unexpectedly, EcR contacts the dMi-2 ATPase domain and increases the efficiency of dMi-2-mediated nucleosome remodelling. This study identifies a non-canonical EcR-corepressor complex with the potential for a direct regulation of ATP-dependent nucleosome remodelling by a nuclear hormone receptor.

Date: 2017
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DOI: 10.1038/ncomms14806

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