Figure 7
mTORC1 inhibition globally increases ER-mitochondria contacts, while ER stress exerts a localized effect.
mTORC1 inhibition mediated by rapamycin induces a global stress response, characterized by an increase in PACS2-mitochondria interaction that leads to a global increase in ER-mitochondria proximity and enhanced mitochondrial Ca2+ uptake throughout the whole cytoplasm. ER stress, on the other hand, induces a local response, characterized by a perinuclear increase in Mfn2-mitochondria interaction and a loss of CNX-mitochondria interaction in the cell periphery. This leads to a local increase in ER-mitochondria contacts, concomitant with increased mitochondrial Ca2+ uptake and bioenergetics.
