KAT5-mediated SOX4 acetylation orchestrates chromatin remodeling during myoblast differentiation

Cell Death Dis. 2015 Aug 20;6(8):e1857. doi: 10.1038/cddis.2015.190.

S-M Jang ¹, J-W Kim ¹, C-H Kim ¹, J-H An ¹, A Johnson ², P I Song ³, S Rhee ¹, K-H Choi ¹

Affiliations

1 Department of Life Science, Chung-Ang University, Seoul 156-756, Korea.
2 Department of Dermatology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
3 Department of Dermatology, University of Colorado Denver Anschutz Medical Campus, Aurora, CO 80045, USA.

PMID: 26291311 DOI: 10.1038/cddis.2015.190

Abstract

Transcription factor SOX4 has been implicated in skeletal myoblast differentiation through the regulation of Cald1 gene expression; however, the detailed molecular mechanism underlying this process is largely unknown. Here, we demonstrate that SOX4 acetylation at lysine 95 by KAT5 (also known as Tip60) is essential for Cald1 promoter activity at the onset of C2C12 myoblast differentiation. KAT5 chromodomain was found to facilitate SOX4 recruitment to the Cald1 promoter, which is involved in chromatin remodeling at the promoter. Chromatin occupancy analysis of SOX4, KAT5, and HDAC1 indicated that the expression of putative SOX4 target genes during C2C12 myoblast differentiation is specifically regulated by the molecular switching of the co-activator KAT5 and the co-repressor HDAC1 on SOX4 transcriptional activation.

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