Abstract
Lysine (Lys) is essential for skeletal muscle growth and protein synthesis in mammals. However, the regulatory network underlying Lys-regulated skeletal muscle development is unknown. To determine whether any cross-talk occurs among mammalian targets of rapamycin complex 1 (mTORC1) and Lys in the regulation of muscle satellite cells (SCs) proliferation, we applied the treatment rapamycin (a mTORC1 inhibitor) and MHY1485 (a mTORC1 activator) on Lys-added or -deficient SCs. The results show Lys deprivation significantly decreases SCs viability, protein synthesis, and cell cycling, increases autophagy and apoptosis, and inhibits the mTORC1 signaling pathway. Restoration of Lys content significantly attenuates this effect. mTORC1 signaling pathway activation during Lys deprivation or mTORC1 signaling pathway inhibition during Lys addition attenuates the effect of Lys deprivation or addition on SCs viability, protein synthesis, cell cycling, autophagy, and apoptosis. In conclusion, Lys could improve SCs proliferation, and inhibit SCs apoptosis and autophagy, via the mTORC1 signaling pathway.