Department of Neuroscience, Weinberg Unit for ALS Research, and Farber Institute for Neurosciences, Thomas Jefferson University, Philadelphia, Pennsylvania 19107.
Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138.
J Biol Chem. 2010 Aug 27;285(35):27411-27417. doi: 10.1074/jbc.M110.131243. Epub 2010 Jun 15.
Potassium fluxes integrate mitochondria into cellular activities, controlling their volume homeostasis and structural integrity in many pathophysiological mechanisms. The outer mitochondrial membrane (OMM) is thought to play a passive role in this process because K(+) is believed to equilibrate freely between the cytosol and mitochondrial intermembrane space. By patch clamping mitochondria isolated from the central nervous systems of adult mitoCFP transgenic mice, we discovered the existence of I(OMMKi), a novel voltage-dependent inwardly rectifying K(+) conductance located in the OMM. I(OMMKi) is regulated by osmolarity, potentiated by cAMP, and activated at physiological negative potentials, allowing K(+) to enter the mitochondrial intermembrane space in a controlled regulated fashion. The identification of I(OMMKi) in the OMM supports the notion that a membrane potential could exist across this membrane in vivo and suggests that the OMM possesses regulated pathways for K(+) uptake.
钾通量将线粒体整合到细胞活动中,在许多病理生理机制中控制其体积平衡和结构完整性。人们认为外线粒体膜(OMM)在此过程中起被动作用,因为 K(+) 被认为可以在细胞质和线粒体膜间隙之间自由平衡。通过对成年 mitoCFP 转基因小鼠中枢神经系统分离的线粒体进行膜片钳钳制,我们发现了 I(OMMKi)的存在,这是一种位于 OMM 的新型电压依赖性内向整流 K(+)电导。I(OMMKi)受渗透压调节,cAMP 增强,并在生理负电位下激活,允许 K(+)以受控的方式进入线粒体膜间隙。在 OMM 中鉴定出 I(OMMKi)支持了这样一种观点,即在体内这个膜上可能存在膜电位,并表明 OMM 具有受调控的 K(+)摄取途径。