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

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 Karas, Hubert Serve, Ewgenij Proschak and Jörn Lausen ()
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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
Ingo Backert: Georg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy
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
Ewgenij Proschak: Institute of Pharmaceutical Chemistry, Johann-Wolfgang-Goethe University
Jörn Lausen: Georg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy

Nature Communications, 2014, vol. 5, issue 1, 1-12

Abstract: 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.

Date: 2014
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DOI: 10.1038/ncomms4995

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