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. 2019 Jan 8;20(3):e47468. doi: 10.15252/embr.201847468

Figure 9. Proposed model of Myoparr function during myogenesis.

Figure 9

Although Ddx17 and PCAF bind to the myogenin promoter, the interaction between Ddx17 and PCAF is weak in the absence of Myoparr. Thus, occupancies of both Ddx17 and PCAF on the myogenin promoter are not sufficient for maximum Pol II recruitment to the myogenin promoter. After binding to the myogenin promoter, Myoparr interacts with Ddx17 to promote the Ddx17‐PCAF interaction. Enhanced Ddx17‐PCAF interaction by Myoparr may be sufficient for maximum Pol II recruitment to the myogenin promoter. Thus, Myoparr is required for specification of myoblast lineage into myogenic differentiation through the Myoparr (upstream) and myogenin (downstream) pathway. In addition, Myoparr is involved in the regulation of myoblast cell cycle withdrawal by activating the expression of myogenic regulatory miRNAs in a myogenin‐independent manner.