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Elife. 2016 Feb 25;5. pii: e12534. doi: 10.7554/eLife.12534.

TBP/TFIID-dependent activation of MyoD target genes in skeletal muscle cells.

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Development, Aging and Regeneration Program, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, United States.
Fondazione Santa Lucia - Istituto di Ricovero e Cura a Carattere Scientifico, Rome, Italy.
Cellular Signaling and Nuclear Dynamics Program, Institut de Génétique et de Biologie Moléculaire et Cellulaire, CU de Strasbourg, France.


Change in the identity of the components of the transcription pre-initiation complex is proposed to control cell type-specific gene expression. Replacement of the canonical TFIID-TBP complex with TRF3/TBP2 was reported to be required for activation of muscle-gene expression. The lack of a developmental phenotype in TBP2 null mice prompted further analysis to determine whether TBP2 deficiency can compromise adult myogenesis. We show here that TBP2 null mice have an intact regeneration potential upon injury and that TBP2 is not expressed in established C2C12 muscle cell or in primary mouse MuSCs. While TFIID subunits and TBP are downregulated during myoblast differentiation, reduced amounts of these proteins form a complex that is detectable on promoters of muscle genes and is essential for their expression. This evidence demonstrates that TBP2 does not replace TBP during muscle differentiation, as previously proposed, with limiting amounts of TFIID-TBP being required to promote muscle-specific gene expression.


TBP; TFIID; cell biology; chromosomes; genes; human; mouse; muscle differentiation; muscle regeneration; myoD; transcription

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