MTORC1 signalling is not essential for the maintenance of muscle mass and function in adult sedentary mice.

ABSTRACT:

Background

The balance between protein synthesis and degradation (proteostasis) is a determining factor for muscle size and function. Signalling via the mammalian target of rapamycin complex 1 (mTORC1) regulates proteostasis in skeletal muscle by affecting protein synthesis and autophagosomal protein degradation. Indeed, genetic inactivation of mTORC1 in developing and growing muscle causes atrophy resulting in a lethal myopathy. However, systemic dampening of mTORC1 signalling by its allosteric inhibitor rapamycin is beneficial at the organismal level and increases lifespan. Whether the beneficial effect of rapamycin comes at the expense of muscle mass and function is yet to be established.

Methods

We conditionally ablated the gene coding for the mTORC1-essential component

SUBMITTER: Ham AS 

PROVIDER: S-EPMC7015237 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature