@article {2393,
	title = {MyoD targets TAF3/TRF3 to activate myogenin transcription.},
	journal = {Molecular Cell},
	volume = {32},
	year = {2008},
	month = {2008 Oct 10},
	pages = {96-105},
	abstract = {<p>Skeletal muscle differentiation requires a cascade of transcriptional events to control the spatial and temporal expression of muscle-specific genes. Until recently, muscle-specific transcription was primarily attributed to prototypic enhancer-binding factors, while the role of core promoter recognition complexes in directing myogenesis remained unknown. Here, we report the development of a purified reconstituted system to analyze the properties of a TAF3/TRF3 complex in directing transcription initiation at the Myogenin promoter. Importantly, this new complex is required to replace the canonical TFIID to recapitulate MyoD-dependent activation of Myogenin. In vitro and cell-based assays identify a domain of TAF3 that mediates coactivator functions targeted by MyoD. Our findings also suggest changes to CRSP/Mediator in terminally differentiated myotubes. This switching of the core promoter recognition complex during myogenesis allows a more balanced division of labor between activators and TAF coactivators, thus providing another strategy to accommodate cell-specific regulation during metazoan development.</p>
},
	keywords = {Animals, Cell Line, Genetic, Homeodomain Proteins, Mice, Multiprotein Complexes, Muscle Fibers, MyoD Protein, Myogenin, Promoter Regions, Protein Structure, Protein Subunits, Recombinant Proteins, Skeletal, TATA Box Binding Protein-Like Proteins, Tertiary, Trans-Activators, Transcription Factor TFIID, Transcription Initiation Site, Transcriptional Activation},
	issn = {1097-4164},
	doi = {10.1073/pnas.1100640108},
	author = {Deato, Maria Divina E and Marr, Michael T and Sottero, Theo and Inouye, Carla and Hu, Ping and Tjian, Robert}
}
@article {2403,
	title = {Switching of the core transcription machinery during myogenesis.},
	journal = {Genes \& Development},
	volume = {21},
	year = {2007},
	month = {2007 Sep 1},
	pages = {2137-49},
	abstract = {<p>Transcriptional mechanisms that govern cellular differentiation typically include sequence-specific DNA-binding proteins and chromatin-modifying activities. These regulatory factors are assumed necessary and sufficient to drive both divergent programs of proliferation and terminal differentiation. By contrast, potential contributions of the basal transcriptional apparatus to orchestrate cell-specific gene expression have been poorly explored. In order to probe alternative mechanisms that control differentiation, we have assessed the fate of the core promoter recognition complex, TFIID, during skeletal myogenesis. Here we report that differentiation of myoblast to myotubes involves the disruption of the canonical holo-TFIID and replacement by a novel TRF3/TAF3 (TBP-related factor 3/TATA-binding protein-associated factor 3) complex. This required switching of core promoter complexes provides organisms a simple yet effective means to selectively turn on one transcriptional program while silencing many others. Although this drastic but parsimonious transcriptional switch had previously escaped our attention, it may represent a more general mechanism for regulating cell type-specific terminal differentiation.</p>
},
	keywords = {Animals, Cell Differentiation, Cell Line, Developmental, Gene Expression Regulation, Genetic, Humans, Mice, Models, Muscle, Muscle Development, Muscle Fibers, Myofibrils, Nuclear Proteins, RNA Interference, Skeletal, TATA Box Binding Protein-Like Proteins, Transcription, Transcription Factor TFIID},
	issn = {0890-9369},
	doi = {10.1073/pnas.1100640108},
	author = {Deato, Maria Divina E and Tjian, Robert}
}
