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EEF1A1 deacetylation enables transcriptional activation of remyelination

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Listed:
  • Mert Duman

    (University of Fribourg
    Johannes Gutenberg University Mainz)

  • Adrien Vaquié

    (University of Fribourg)

  • Gianluigi Nocera

    (University of Fribourg
    Johannes Gutenberg University Mainz)

  • Manfred Heller

    (Proteomics and Mass Spectrometry Core Facility, Department for BioMedical Research, University of Bern)

  • Michael Stumpe

    (University of Fribourg)

  • Devanarayanan Siva Sankar

    (University of Fribourg)

  • Jörn Dengjel

    (University of Fribourg)

  • Dies Meijer

    (Center for Discovery Brain Sciences, Edinburgh Medical School, University of Edinburgh)

  • Teppei Yamaguchi

    (FMI for Biomedical Research, Novartis Research Foundation)

  • Patrick Matthias

    (FMI for Biomedical Research, Novartis Research Foundation)

  • Thomas Zeis

    (University Hospital Basel)

  • Nicole Schaeren-Wiemers

    (University Hospital Basel)

  • Antoinette Hayoz

    (University of Fribourg)

  • Sophie Ruff

    (University of Fribourg)

  • Claire Jacob

    (University of Fribourg
    Johannes Gutenberg University Mainz)

Abstract

Remyelination of the peripheral and central nervous systems (PNS and CNS, respectively) is a prerequisite for functional recovery after lesion. However, this process is not always optimal and becomes inefficient in the course of multiple sclerosis. Here we show that, when acetylated, eukaryotic elongation factor 1A1 (eEF1A1) negatively regulates PNS and CNS remyelination. Acetylated eEF1A1 (Ac-eEF1A1) translocates into the nucleus of myelinating cells where it binds to Sox10, a key transcription factor for PNS and CNS myelination and remyelination, to drag Sox10 out of the nucleus. We show that the lysine acetyltransferase Tip60 acetylates eEF1A1, whereas the histone deacetylase HDAC2 deacetylates eEF1A1. Promoting eEF1A1 deacetylation maintains the activation of Sox10 target genes and increases PNS and CNS remyelination efficiency. Taken together, these data identify a major mechanism of Sox10 regulation, which appears promising for future translational studies on PNS and CNS remyelination.

Suggested Citation

  • Mert Duman & Adrien Vaquié & Gianluigi Nocera & Manfred Heller & Michael Stumpe & Devanarayanan Siva Sankar & Jörn Dengjel & Dies Meijer & Teppei Yamaguchi & Patrick Matthias & Thomas Zeis & Nicole Sc, 2020. "EEF1A1 deacetylation enables transcriptional activation of remyelination," Nature Communications, Nature, vol. 11(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-17243-z
    DOI: 10.1038/s41467-020-17243-z
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