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A role for histone deacetylase HDAC1 in modulating the transcriptional activity of MyoD: inhibition of the myogenic program.

The EMBO journal | Apr 2, 2001

http://www.ncbi.nlm.nih.gov/pubmed/11285237

The molecular mechanism(s) that are responsible for suppressing MyoD's transcriptional activities in undifferentiated skeletal muscle cells have not yet been determined. We now show that MyoD associates with a histone deacetylase-1 (HDAC1) in these cells and that this interaction is responsible for silencing MyoD-dependent transcription of endogenous p21 as well as muscle-specific genes. Specifically, we present evidence that HDAC1 can bind directly to MyoD and use an acetylated MyoD as a substrate in vitro, whereas a mutant version of HDAC1 (H141A) can not. Further more, this mutant also fails to repress MyoD-mediated transcription in vivo, and unlike wild-type HDAC1 it can not inhibit myogenic conversion, as judged by confocal microscopy. Finally, we show that an endogenous MyoD can be acetylated upon its conversion to a hypophosphorylated state and only when the cells have been induced to differentiate. These results provide for a model which postulates that MyoD may be co-dependent on HDAC1 and P/CAF for temporally controlling its transcriptional activity before and after the differentiation of muscle cells.

Pubmed ID: 11285237 RIS Download

Mesh terms: Acetylation | Acetyltransferases | Animals | Cell Cycle Proteins | Cell Differentiation | Cell Line | Cell Line, Transformed | Cyclin-Dependent Kinase Inhibitor p21 | Cyclins | Histone Acetyltransferases | Histone Deacetylase 1 | Histone Deacetylases | Humans | Jurkat Cells | Mice | Muscle, Skeletal | MyoD Protein | Nuclear Proteins | Promoter Regions, Genetic | Trans-Activators | Transcription Factors | Transcription, Genetic | p300-CBP Transcription Factors

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