Mitochondrial respiration links TOR complex 2 signaling to calcium regulation and autophagy. Issue 7 (3rd July 2017)

• Record Type: Journal Article
• Authors: Vlahakis, Ariadne; Lopez Muniozguren, Nerea; Powers, Ted
• Is Part Of: Autophagy. Volume 13:Issue 7(2017)
• Page Start: 1256
• Page End: 1257
• Publication Date: 2017-07-03
• Subjects: amino acid -- calcineurin -- calcium -- endoplasmic reticulum -- GAAC -- Mid1 -- mitochondria -- reactive oxygen species (ROS) -- TORC1 -- TORC2 -- Ypk1; Autophagic vacuoles -- Periodicals; Apoptosis -- Periodicals; Cell death -- Periodicals; Lysosomes -- Periodicals; Degeneration (Pathology) -- Periodicals; Autophagy -- Periodicals; Cell Death -- Periodicals; Lysosomes -- Periodicals; Periodicals; 571.936
• DOI: 10.1080/15548627.2017.1299314
• Languages: English
• ISSNs: 1554-8627

Abstract

ABSTRACT: The target of rapamycin (TOR) kinase is a conserved regulator of cell growth and functions within 2 different protein complexes, TORC1 and TORC2, where TORC2 positively controls macroautophagy/autophagy during amino acid starvation. Under these conditions, TORC2 signaling inhibits the activity of the calcium-regulated phosphatase calcineurin and promotes the general amino acid control (GAAC) response and autophagy. Here we demonstrate that TORC2 regulates calcineurin by controlling the respiratory activity of mitochondria. In particular, we find that mitochondrial oxidative stress affects the calcium channel regulatory protein Mid1, which we show is an essential upstream activator of calcineurin. Thus, these findings describe a novel regulation for autophagy that involves TORC2 signaling, mitochondrial respiration, and calcium homeostasis.