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. 2018 Mar 26;37(8):e98239. doi: 10.15252/embj.201798239

Figure 7. Constitutive activation of p110α in MuSCs from uninjured muscles led to their spontaneous quiescence exit and gradual depletion.

Figure 7

  1. Top: the experimental scheme. Adult Ctrl and ip110αca mice (n = 3 in each group) were injected with Tmx and EdU as indicated and sacrificed 3 days after the last dose of EdU. FACS‐isolated MuSCs were fixed immediately and stained with EdU (green), Pax7 (red) and DAPI (blue). Arrowheads: EdU+ MuSCs.
  2. Quantification of the EdU+ MuSCs in (A) by counting ˜600 MuSCs/mouse.
  3. TA muscle sections from the Ctrl and ip110αca mice (n = 3) at different time points after the Tmx treatment were stained for YFP (red), laminin (green), and DAPI (blue). Representative images are shown. Arrows: YFP+ MuSCs.
  4. Quantification of the YFP+ MuSCs in (C) by counting ˜600 MuSCs/mouse.
  5. The relative mRNA levels of Myod and Myogenin in MuSCs from (A) were measured by RT–qPCR (n = 3).
  6. A schematic showing that PI3K regulates quiescence exit and the cell cycle re‐entry in MuSCs via both mTORC1‐c‐Jun and FoxOs.
Data information: Scale bars: 25 μm. In (B, D, E), the data are presented as mean ± s.d. **P < 0.01; ***P < 0.001; unpaired Student's t‐test.