Nfix Induces a Switch in Sox6 Transcriptional Activity to Regulate MyHC-I 
Expression in Fetal Muscle

Taglietti, Valentina; Maroli, Giovanni; Cermenati, Solei; Monteverde, Stefania; Ferrante, Andrea; Rossi, Giuliana; Cossu, Giulio; Beltrame, Monica; Messina, Graziella

doi:10.1016/j.celrep.2016.10.082

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Nfix Induces a Switch in Sox6 Transcriptional Activity to Regulate MyHC-I Expression in Fetal Muscle

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Maroli, Giovanni
Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Citation

Taglietti, V., Maroli, G., Cermenati, S., Monteverde, S., Ferrante, A., Rossi, G., et al. (2016). Nfix Induces a Switch in Sox6 Transcriptional Activity to Regulate MyHC-I Expression in Fetal Muscle. CELL REPORTS, 17(9), 2354-2366. doi:10.1016/j.celrep.2016.10.082.

Cite as: https://hdl.handle.net/21.11116/0000-0001-BD6B-3

Abstract

Sox6 belongs to the Sox gene family and plays a pivotal role in fiber type differentiation, suppressing transcription of slow-fiber-specific genes during fetal development. Here, we show that Sox6 plays opposite roles in MyHC-I regulation, acting as a positive and negative regulator of MyHC-I expression during embryonic and fetal myogenesis, respectively. During embryonic myogenesis, Sox6 positively regulates MyHC-I via transcriptional activation of Mef2C, whereas during fetal myogenesis, Sox6 requires and cooperates with the transcription factor Nfix in repressing MyHC-I expression. Mechanistically, Nfix is necessary for Sox6 binding to the MyHC-I promoter and thus for Sox6 repressive function, revealing a key role for Nfix in driving Sox6 activity. This feature is evolutionarily conserved, since the orthologs Nfixa and Sox6 contribute to repression of the slow-twitch phenotype in zebrafish embryos. These data demonstrate functional cooperation between Sox6 and Nfix in regulating MyHC-I expression during prenatal muscle development.