TBP/TFIID-dependent activation of MyoD target genes in skeletal muscle cells.
Barbora MalecovaAlessandra Dall'AgneseLuca MadaroSole GattoPaula Coutinho TotoSonia AlbiniTammy RyanLàszlò ToraPier Lorenzo PuriPublished in: eLife (2016)
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.
Keyphrases
- skeletal muscle
- gene expression
- dna methylation
- stem cells
- insulin resistance
- genome wide
- high fat diet induced
- single cell
- adipose tissue
- risk assessment
- oxidative stress
- metabolic syndrome
- transcription factor
- mesenchymal stem cells
- young adults
- replacement therapy
- bioinformatics analysis
- genome wide identification
- genome wide analysis