Journal
CELL
Volume 140, Issue 4, Pages 554-566Publisher
CELL PRESS
DOI: 10.1016/j.cell.2010.01.027
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Funding
- EC
- ERC
- Ministry of Research (FIRB) and of Health
- Telethon
- AFM
- Fondazione Roma
- Duchenne Parent Project (Italy)
- NASA [NNJ06HA59]
- NIHLBI [H080624]
- NIH [AR052777]
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Skeletal myogenesis, like hematopoiesis, occurs in successive developmental stages that involve different cell populations and expression of different genes. We show here that the transcription factor nuclear factor one X (Nfix), whose expression is activated by Pax7 in fetal muscle, in turn activates the transcription of fetal specific genes such as MCK and beta-enolase while repressing embryonic genes such as slow myosin. In the case of the MCK promoter, Nfix forms a complex with PKC theta that binds, phosphorylates, and activates MEF2A. Premature expression of Nfix activates fetal and suppresses embryonic genes in embryonic muscle, whereas muscle-specific ablation of Nfix prevents fetal and maintains embryonic gene expression in the fetus. Therefore, Nfix acts as a transcriptional switch from embryonic to fetal myogenesis.
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