TBP/TFIID-dependent activation of MyoD target genes in skeletal muscle cells
Abstract
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.
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Author details
Reviewing Editor
- Alan G Hinnebusch, National Institute of Child Health and Human Development, United States
Ethics
Animal experimentation: This study was performed in strict accordance with the recommendations in the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health. All of the animals were handled according to approved institutional animal care and use committee (IACUC) protocols (#13-007) of the Sanford Burnham Prebys Medical Discovery Institute. Every effort was made to minimize suffering.
Version history
- Received: October 26, 2015
- Accepted: January 21, 2016
- Accepted Manuscript published: February 11, 2016 (version 1)
- Version of Record published: February 25, 2016 (version 2)
Copyright
© 2016, Malecova et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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