Department of Cellular and Physiological Sciences, University of British Columbia, 2350 Health Sciences Mall, Vancouver, BC, Canada.
Protoplasma. 2012 Feb;249 Suppl 1:S49-58. doi: 10.1007/s00709-011-0349-3. Epub 2011 Nov 22.
Nanometre-scale spaces between organelles represent focused nodes for signal transduction and the control of cellular decisions. The endoplasmic reticulum (ER) and the mitochondria form dynamic quasi-synaptic interaction nanodomains in all cell types examined, but the functional role of these junctions in cellular metabolism and cell survival remains to be fully understood. In this paper, we review recent evidence that ER Ca(2+) channels, such as the RyR and IP(3)R, can signal specifically across this nanodomain to the adjacent mitochondria to pace basal metabolism, with focus on the pancreatic β-cell. Blocking these signals in the basal state leads to a form of programmed cell death associated with reduced ATP and the induction of calpain-10 and hypoxia-inducible factors. On the other hand, the hyperactivity of this signalling domain plays a deleterious role during classical forms of apoptosis. Thus, the nanospace between ER and mitochondria represents a critical rheostat controlling both metabolism and programmed cell death. Many aspects of the mechanisms underlying this control system remain to be uncovered, and new nanotechnologies are required understand these domains at a molecular level.
细胞器之间的纳米空间代表信号转导和细胞决策控制的聚焦节点。内质网 (ER) 和线粒体在所有检查过的细胞类型中形成动态拟突触相互作用纳米域,但这些连接在细胞代谢和细胞存活中的功能作用仍有待充分理解。在本文中,我们回顾了最近的证据,表明 ER Ca(2+) 通道,如 RyR 和 IP(3)R,可以特异性地跨越这个纳米域传递信号到相邻的线粒体,以调节基础代谢,重点是胰腺β细胞。在基础状态下阻断这些信号会导致与 ATP 减少和钙蛋白酶-10 和缺氧诱导因子诱导相关的一种程序性细胞死亡形式。另一方面,该信号域的过度活跃在经典形式的细胞凋亡中起有害作用。因此,ER 和线粒体之间的纳米空间代表了控制代谢和程序性细胞死亡的关键变阻器。该控制系统的许多机制仍有待揭示,需要新的纳米技术来在分子水平上理解这些域。