A dual role of linker histone H1.4 Lys 34 acetylation in transcriptional activation (original) (raw)

  1. Annalisa Izzo1,2,9,
  2. Miroslav Dundr3,
  3. Philipp Tropberger1,
  4. Luka Ozretić4,
  5. Jutta Kirfel5,
  6. Elisabeth Scheer2,
  7. Philippe Tropel2,
  8. Jacek R. Wiśniewski6,
  9. Laszlo Tora2,
  10. Stephane Viville2,7,
  11. Reinhard Buettner4 and
  12. Robert Schneider1,2,8,10
  13. 1Max Planck Institute of Immunobiology and Epigenetics, 79108 Freiburg, Germany;
  14. 2Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS UMR 7104, INSERM U 964, Université de Strasbourg, 67404 Illkirch, France;
  15. 3Department of Cell Biology, Rosalind Franklin University of Medicine and Science, North Chicago Illinois 60064, USA;
  16. 4Institute for Pathology, University Cologne, 50924 Cologne, Germany;
  17. 5Institute of Pathology, University Bonn, 53125 Bonn, Germany;
  18. 6Department of Proteomics and Signal Trasduction, Max Planck Institute for Biochemistry, 82152 Martinsried, Germany;
  19. 7Centre Hospitalier Universitaire, 67200 Strasbourg, France;
  20. 8BIOSS Centre for Biological Signalling Studies, Albert-Ludwigs-Universität, 79104 Freiburg, Germany
  21. ↵9 These authors contributed equally to this work.

Abstract

The linker histone H1 is a key player in chromatin organization, yet our understanding of the regulation of H1 functions by post-translational modifications is very limited. We provide here the first functional characterization of H1 acetylation. We show that H1.4K34 acetylation (H1.4K34ac) is mediated by GCN5 and is preferentially enriched at promoters of active genes, where it stimulates transcription by increasing H1 mobility and recruiting a general transcription factor. H1.4K34ac is dynamic during spermatogenesis and marks undifferentiated cells such as induced pluripotent stem (iPS) cells and testicular germ cell tumors. We propose a model for H1.4K34ac as a novel regulator of chromatin function with a dual role in transcriptional activation.

Footnotes