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PADI4 acts as a coactivator of Tal1 by counteracting repressive histone arginine methylation

Author

Listed:
  • Stephan Kolodziej

    (Georg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy)

  • Olga N. Kuvardina

    (Georg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy)

  • Thomas Oellerich

    (Hematology/Oncology, Johann-Wolfgang-Goethe University)

  • Julia Herglotz

    (Georg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy
    Present address: Heinrich-Pette-Institute, Leibniz Institute for Experimental Virology, Martinistrasse 52, D-20251 Hamburg, Germany)

  • Ingo Backert

    (Georg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy
    Present address: University Hospital Erlangen, Kussmaul Campus for Medical Research, Hartmannstrasse 14, D-91052 Erlangen, Germany)

  • Nicole Kohrs

    (Georg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy)

  • Estel.la Buscató

    (Institute of Pharmaceutical Chemistry, Johann-Wolfgang-Goethe University)

  • Sandra K. Wittmann

    (Institute of Pharmaceutical Chemistry, Johann-Wolfgang-Goethe University)

  • Gabriela Salinas-Riester

    (Medical-University Goettingen, Transcriptome Analysis Laboratory)

  • Halvard Bonig

    (German Red Cross Blood Service and Institute for Transfusion Medicine and Immunohematology, Johann-Wolfgang-Goethe University)

  • Michael Karas

    (Institute of Pharmaceutical Chemistry, Johann-Wolfgang-Goethe University)

  • Hubert Serve

    (Hematology/Oncology, Johann-Wolfgang-Goethe University
    German Cancer Consortium (DKTK))

  • Ewgenij Proschak

    (Institute of Pharmaceutical Chemistry, Johann-Wolfgang-Goethe University
    German Cancer Consortium (DKTK))

  • Jörn Lausen

    (Georg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy)

Abstract

The transcription factor Tal1 is a critical activator or repressor of gene expression in hematopoiesis and leukaemia. The mechanism by which Tal1 differentially influences transcription of distinct genes is not fully understood. Here we show that Tal1 interacts with the peptidylarginine deiminase IV (PADI4). We demonstrate that PADI4 can act as an epigenetic coactivator through influencing H3R2me2a. At the Tal1/PADI4 target gene IL6ST the repressive H3R2me2a mark triggered by PRMT6 is counteracted by PADI4, which augments the active H3K4me3 mark and thus increases IL6ST expression. In contrast, at the CTCF promoter PADI4 acts as a repressor. We propose that the influence of PADI4 on IL6ST transcription plays a role in the control of IL6ST expression during lineage differentiation of hematopoietic stem/progenitor cells. These results open the possibility to pharmacologically influence Tal1 in leukaemia.

Suggested Citation

  • Stephan Kolodziej & Olga N. Kuvardina & Thomas Oellerich & Julia Herglotz & Ingo Backert & Nicole Kohrs & Estel.la Buscató & Sandra K. Wittmann & Gabriela Salinas-Riester & Halvard Bonig & Michael Kar, 2014. "PADI4 acts as a coactivator of Tal1 by counteracting repressive histone arginine methylation," Nature Communications, Nature, vol. 5(1), pages 1-12, September.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4995
    DOI: 10.1038/ncomms4995
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