Nerve activity inhibits mTORC1-dependent protein synthesis in skeletal muscle

To find out intracellular signaling pathways regulting fiber type specific muscle wasting we generated a new mouse model, which allows us to label specifically muscle proteins. Interestingly, we observed that loss of muscle activity by denervation induces a strong increase of protein labeling in oxidative, mitochondria-rich muscle fibers. MS-based analysis, rapamycin treatments and genetic models showed requirement of mTORC1 signaling for increased protein synthesis in dependence of nerve activity.