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Fig. 1 | Skeletal Muscle

Fig. 1

From: The Notch signaling network in muscle stem cells during development, homeostasis, and disease

Fig. 1

The Notch signaling pathway during myogenic progression and self-renewal. A Basic scheme of the Notch signaling pathway in murine muscle cells. The receptor is more highly expressed on the stem/progenitor cell (signal receiving cell), whereas the DLL ligands on the committed myoblasts and the mature myofibers (signal sending cells). Ligand-receptor interaction triggers intramembrane proteolysis and release of the intracellular domain of Notch (NICD). NICD then translocates into the nucleus where it forms a complex with its main downstream effector and DNA binding transcription factor RBPJ, and members of the coactivator Mastermind-like (MAML) family. The triprotein NICD transcriptional complex recruits additional coactivators and histone modifiers to activate transcription, not illustrated here for simplicity. B During MuSC activation and myogenic commitment, Notch signaling activity is downregulated. Quiescent MuSCs have high Notch activity (dark blue in color key), which maintains Pax7 and inhibits Myod and Myogenin expression. Immediately after MuSC activation, Notch activity rapidly declines and the cells express MYOD, which accelerates S-phase entry. During the proliferation phase, high Notch activity is restricted to some cells, which remain undifferentiated and self-renew to replenish the satellite cell pool (dotted arrow). Notch activation is principally triggered by ligand-bearing differentiating myoblasts (block arrow indicates direction of Notch signaling). Mature myofibers, in which Notch activity is insignificant (green color in color key), are the main source of ligand in the resting muscle and maintain MuSC quiescence by direct cell-cell interaction (block arrow)

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