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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.
Highlights
TFs initiate and execute myoblast differentiation together with histone-modifying enzymes.[8,9] myogenic differentiation (MyoD)-centered transcriptional regulation via molecular switching between repressors and activators is well studied during myoblast differentiation.[5]
SRY-box 4 (SOX4) acetylation is regulated by K acetyltransferase 5 (KAT5) during myoblast differentiation
KAT5-Y47A mutant showed deficient differentiation rates (Supplementary Figure 5) together with decreased acetylation rates of SOX4 and SOX4 interaction compared with KAT5-wild type (WT) (Figure 6s, lanes 3 and 4). These results suggest that chromatin remodeling mediated by KAT5 is required for SOX4–KAT5 interaction and KAT5-mediated SOX4 acetylation, resulting in SOX4-dependent Cald[1] promoter activation during myoblast differentiation
Summary
TFs initiate and execute myoblast differentiation together with histone-modifying enzymes.[8,9] MyoD-centered transcriptional regulation via molecular switching between repressors and activators is well studied during myoblast differentiation.[5] In undifferentiated myoblasts, HDAC1 interacts with MyoD. This interaction maintains chromatin in a compact structure by preventing histone hyperacetylation at the response elements of muscle genes, which inhibits MyoD loading on target genes in undifferentiated myoblasts.[1,10] Differentiation cues promote.
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