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

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  • Judith Kreher

    (Institute of Molecular Biology and Tumour Research, Philipps University Marburg
    Present address: Roche Diagnostics Deutschland GmbH, Mannheim 68305, Germany)

  • 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
    Present address: Institute of Molecular Biology, Mainz 55128, Germany)

  • Erik Engelen

    (Institute of Molecular Biology and Tumour Research, Philipps University Marburg
    Present address: Roche Diagnostics Deutschland GmbH, Mannheim 68305, Germany)

  • Roman Pahl

    (Institute of Medical Biometry and Epidemiology, Philipps University Marburg
    Present address: GSK Marburg Vaccines and Diagnostics, Marburg 35041, Germany)

  • Florian Finkernagel

    (Center for Tumour Biology and Immunology, Philipps University Marburg)

  • Magdalena Murawska

    (Institute of Molecular Biology and Tumour Research, Philipps University Marburg
    Present address: Biomedical Center Munich, Ludwig Maximilians University, Planegg-Martinsried 82152, Germany)

  • Ikram Ullah

    (Institute of Molecular Biology and Tumour Research, Philipps University Marburg)

  • Alexander Brehm

    (Institute of Molecular Biology and Tumour Research, Philipps University Marburg)

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.

Suggested Citation

  • Judith Kreher & Kristina Kovač & Karim Bouazoune & Igor Mačinković & Anna Luise Ernst & Erik Engelen & Roman Pahl & Florian Finkernagel & Magdalena Murawska & Ikram Ullah & Alexander Brehm, 2017. "EcR recruits dMi-2 and increases efficiency of dMi-2-mediated remodelling to constrain transcription of hormone-regulated genes," Nature Communications, Nature, vol. 8(1), pages 1-13, April.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14806
    DOI: 10.1038/ncomms14806
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