Regulation of skeletal myogenesis by association of the MEF2 transcription factor with class II histone deacetylases

被引:448
作者
Lu, JR [1 ]
McKinsey, TA [1 ]
Zhang, CL [1 ]
Olson, EN [1 ]
机构
[1] Univ Texas, SW Med Ctr, Dept Mol Biol, Dallas, TX 75235 USA
基金
美国国家卫生研究院;
关键词
D O I
10.1016/S1097-2765(00)00025-3
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Skeletal muscle differentiation is controlled by associations between myogenic basic-helix-loop-helix and MEF2 transcription factors. We show that chromatin associated with muscle genes regulated by these transcription factors becomes acetylated during myogenesis and that class II histone deacetylases (HDACs), which interact with MEF2, specifically suppress myoblast differentiation. These HDACs do not interact directly with MyoD, yet they suppress its myogenic activity through association with MEF2. Elevating the level of MyoD can override the repression imposed by HDACs on muscle genes. HDAC-mediated repression of myogenesis also can be overcome by CaM kinase and insulin-like growth factor (IGF) signaling. These findings reveal central roles for HDACs in chromatin remodeling during myogenesis and as intranuclear targets far signaling pathways controlled by IGF and CaM kinase.
引用
收藏
页码:233 / 244
页数:12
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