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Activity-dependent phosphorylation of MeCP2 threonine 308 regulates interaction with NCoR

Author

Listed:
  • Daniel H. Ebert

    (Harvard Medical School, Boston, Massachusetts 02115, USA
    Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA)

  • Harrison W. Gabel

    (Harvard Medical School, Boston, Massachusetts 02115, USA)

  • Nathaniel D. Robinson

    (Harvard Medical School, Boston, Massachusetts 02115, USA)

  • Nathaniel R. Kastan

    (Harvard Medical School, Boston, Massachusetts 02115, USA)

  • Linda S. Hu

    (Harvard Medical School, Boston, Massachusetts 02115, USA)

  • Sonia Cohen

    (Harvard Medical School, Boston, Massachusetts 02115, USA)

  • Adrija J. Navarro

    (Harvard Medical School, Boston, Massachusetts 02115, USA)

  • Matthew J. Lyst

    (Wellcome Trust Centre for Cell Biology, University of Edinburgh)

  • Robert Ekiert

    (Wellcome Trust Centre for Cell Biology, University of Edinburgh)

  • Adrian P. Bird

    (Wellcome Trust Centre for Cell Biology, University of Edinburgh)

  • Michael E. Greenberg

    (Harvard Medical School, Boston, Massachusetts 02115, USA)

Abstract

Rett syndrome is caused by mutations in MeCP2, and this study identifies a site on MeCP2, T308, whose phosphorylation is regulated by neuronal activity: phosphorylation of T308 blocks the interaction of MeCP2 with the NCoR co-repressor complex, suppressing MeCP2's ability to repress transcription, and mice carrying mutations of MeCP2 T308 show Rett-syndrome-related symptoms.

Suggested Citation

  • Daniel H. Ebert & Harrison W. Gabel & Nathaniel D. Robinson & Nathaniel R. Kastan & Linda S. Hu & Sonia Cohen & Adrija J. Navarro & Matthew J. Lyst & Robert Ekiert & Adrian P. Bird & Michael E. Greenb, 2013. "Activity-dependent phosphorylation of MeCP2 threonine 308 regulates interaction with NCoR," Nature, Nature, vol. 499(7458), pages 341-345, July.
    • Handle: RePEc:nat:nature:v:499:y:2013:i:7458:d:10.1038_nature12348
    DOI: 10.1038/nature12348
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