Journal
CELL DISCOVERY
Volume 2, Issue -, Pages -Publisher
SPRINGERNATURE
DOI: 10.1038/celldisc.2016.37
Keywords
differentiation; lysine; muscle; methyltransferase; SETDB1/ESET/KMT1E; Wnt signalling
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Funding
- Association Francaise contre les Myopathies Telethon (AFM-Telethon)
- Institut National du Cancer (INCa)
- Agence Nationale de la Recherche (ANR)
- Fondation Association pour la Recherche sur le Cancer (Fondation ARC)
- Groupement des Entreprises Francaises pour la Lutte contre le Cancer (GEFLUC)
- DIM Stem Pole, Fondation Bettencourt-Schueller
- CNRS
- Universite Paris Diderot
- 'Who Am I?' Laboratory of Excellence - French Government through 'Investments for the Future' programme [ANR-11- LABX-0071, ANR-11-IDEX-0005-01]
- INSERM
- ANR-Jeunes Chercheurs [RPV13010KKA]
- AFM-Telethon
- Fondation ARC
- Mairie de Paris
- Ministere de la Recherche
- ANR
- Who Am I? Labex post-doc fellowship
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The histone 3 lysine 9 methyltransferase Setdb1 is essential for both stem cell pluripotency and terminal differentiation of different cell types. To shed light on the roles of Setdb1 in these mutually exclusive processes, we used mouse skeletal myoblasts as a model of terminal differentiation. Ex vivo studies on isolated single myofibres showed that Setdb1 is required for adult muscle stem cells expansion following activation. In vitro studies in skeletal myoblasts confirmed that Setdb1 suppresses terminal differentiation. Genomic binding analyses showed a release of Setdb1 from selected target genes upon myoblast terminal differentiation, concomitant to a nuclear export of Setdb1 to the cytoplasm. Both genomic release and cytoplasmic Setdb1 relocalisation during differentiation were dependent on canonical Wnt signalling. Transcriptomic assays in myoblasts unravelled a significant overlap between Setdb1 and Wnt3a regulated genetic programmes. Together, our findings revealed Wnt-dependent subcellular relocalisation of Setdb1 as a novel mechanism regulating Setdb1 functions and myogenesis.
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