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    Myogenin and the SWI/SNF ATPase Brg1 maintain myogenic gene expression at different stages of skeletal myogenesis

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    Authors
    Ohkawa, Yasuyuki
    Yoshimura, Saori
    Higashi, Chiduru
    Marfella, Concetta G. A.
    Dacwag, Caroline S.
    Tachibana, Taro
    Imbalzano, Anthony N.
    Student Authors
    Concetta G. A. Marfella
    UMass Chan Affiliations
    Department of Cell Biology
    Document Type
    Journal Article
    Publication Date
    2007-03-02
    Keywords
    Animals; Cell Line; Chromosomal Proteins, Non-Histone; DNA Helicases; Embryo, Mammalian; *Gene Expression Regulation, Developmental; Mice; Muscle Development; Muscle, Skeletal; MyoD Protein; Myogenin; Nuclear Proteins; Promoter Regions (Genetics); Transcription Factors
    Cell Biology
    Life Sciences
    Medicine and Health Sciences
    
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    Link to Full Text
    http://dx.doi.org/10.1074/jbc.M608898200
    Abstract
    Many studies have examined transcriptional regulation during the initiation of skeletal muscle differentiation; however, there is less information regarding transcriptional control during adult myogenesis and during the maintenance of the differentiated state. MyoD and the mammalian SWI/SNF chromatin-remodeling enzymes containing the Brg1 ATPase are necessary to induce myogenesis in cell culture models and in developing embryonic tissue, whereas myogenin and Brg1 are critical for the expression of the late genes that induce terminal muscle differentiation. Here, we demonstrate that myogenin also binds to its own promoter during the late stages of embryonic muscle development. As is the case during embryonic myogenesis, MyoD and Brg1 co-localize to the myogenin promoter in primary adult muscle satellite cells. However, in mature myofibers, myogenin and Brg1 are preferentially co-localized to the myogenin promoter. Thus, the myogenin promoter is occupied by different myogenic factors at different times of myogenesis. The relevance of myogenin in the continued expression from its own promoter is demonstrated in culture, where we show that myogenin, in the absence of MyoD, is capable of maintaining its own expression by recruiting the Brg1 ATPase to modify promoter chromatin structure and facilitate myogenin expression. Finally, we utilized in vivo electroporation to demonstrate that Brg1 is required for the continued production of the myogenin protein in newborn skeletal muscle tissue. These findings strongly suggest that the skeletal muscle phenotype is maintained by myogenin and the continuous activity of Brg1-based SWI/SNF chromatin-remodeling enzymes.
    Source
    J Biol Chem. 2007 Mar 2;282(9):6564-70. Epub 2006 Dec 27. Link to article on publisher's site
    DOI
    10.1074/jbc.M608898200
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/34263
    PubMed ID
    17194702
    Related Resources
    Link to article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1074/jbc.M608898200
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    Morningside GSBS Scholarly Publications

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