期刊
JOURNAL OF MOLECULAR BIOLOGY
卷 428, 期 11, 页码 2329-2343出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jmb.2016.03.029
关键词
EHMT; muscle; differentiation; proliferation; histone methylation
资金
- 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
- CNRS
- Universite Paris Diderot
- Who Am I? Laboratory of Excellence - French Government [ANR-11- LABX-0071, ANR-11-IDEX-0005-01]
- Fondation ARC
- Maine de Paris
- Ministere de la Recherche
- Who Am I? Labex Transition post-doc fellowship
- INCA
- Who Am I? Labex
Lysine methyltransferases G9a and GLP (G9a-like protein) are highly homologous and form functional heterodimeric complexes that establish mono- and dimethylation on histone H3 lysine 9 (H3K9me1, H3K9me2) in euchromatin. Here, we describe unexpected distinct roles for G9a and GLP in skeletal muscle terminal differentiation. Indeed, gain- or loss-of-function assays in myoblasts showed, in agreement with previous reports, that G9a inhibits terminal differentiation. While GLP plays a more intricate role in muscle differentiation,in one hand, both GLP gain and loss of function inhibit late steps of differentiation; on the other hand, in contrast to G9a, GLP overexpression promotes abnormal precocious expression of muscle differentiation-specific genes already in proliferating myoblasts. In agreement, transcriptomic analysis indicates that G9a and GLP regulate different sets of genes. Thus, GLP, but not G9a, inhibits proteasome subunit-encoding genes expression, resulting in an inhibition of the proteasome activities. Subsequently, GLP, but not G9a, overexpression stabilizes MyoD that is likely to be responsible for muscle markers expression in proliferating myoblasts. (C) 2016 Elsevier Ltd. All rights reserved.
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