TY - JOUR
AU - De Stefani, Diego
AB - SummaryMitochondria provide chemical energy for endoergonic reactions in form of ATP. Their activity must meet cellular energy requirements, but mechanisms linking organelle performance to ATP levels are poorly understood. Here, we identify a mitochondria-localized protein complex that mediates ATP-dependent potassium currents, referred to as mitoKATP. We show that similarly to their plasma membrane counterparts, mitoKATP channels are composed of pore-forming (MITOK) and ATP-binding (MITOSUR) subunits. In vitro reconstitution of MITOK together with MITOSUR recapitulates the main properties of mitoKATP. While MITOK overexpression triggers dramatic organelle swelling, its genetic ablation causes instability of mitochondrial membrane potential, widening of intracristal space and decreased oxidative phosphorylation. Most importantly, loss of Mitok suppresses cardioprotection elicited by diazoxide-induced pharmacological preconditioning. Our data indicate that mitoKATP channels respond to the cellular energetic status by regulating organelle volume and function, thereby representing key players in mitochondrial physiology with potential impact on several pathological processes.
TI - Identification of an ATP-sensitive potassium channel in mitochondria
JO - Nature
DO - 10.1038/s41586-019-1498-3
DA - 2019-08-21
UR - https://www.deepdyve.com/lp/pubmed-central/identification-of-an-atp-sensitive-potassium-channel-in-mitochondria-iL04EqM4eB
SP - 609
EP - 613
VL - 572
IS - 7771
DP - DeepDyve
ER -