We find that acute chemical modulation of mTORC1 signaling decreased mitochondrial oxygen consumption, increased mitochondrial membrane potential and reduced susceptibility to stress-induced mitophagy. In cellular models of Friedreich Ataxia (FA), where loss of the Frataxin (FXN) protein suppresses Fe-S cluster synthesis and mitochondrial respiration, the changes induced by mTORC1 inhibitors lead to improved cell survival. Proteomic-based profiling uncover compositional changes that could underlie mTORC1-dependent modulation of FXN-deficient mitochondria.
Thursday, August 8, 2024
mTORC1 Signaling Inhibition Modulates Mitochondrial Function in Frataxin Deficiency
mTORC1 Signaling Inhibition Modulates Mitochondrial Function in Frataxin Deficiency, Madison Lehmer, Roberto Zoncu, bioRxiv 2024.08.06.606942; doi:10.1101/2024.08.06.606942
