线粒体
内质网
细胞生物学
生物
细胞器
钙
细胞凋亡
细胞
生物化学
化学
有机化学
作者
György Csordás,Christian Renken,Péter Várnai,Ludivine Walter,David Weaver,Karolyn Buttle,Tamás Balla,Carmen A. Mannella,György Hajnóczky
标识
DOI:10.1083/jcb.200604016
摘要
The role of mitochondria in cell metabolism and survival is controlled by calcium signals that are commonly transmitted at the close associations between mitochondria and endoplasmic reticulum (ER). However, the physical linkage of the ER-mitochondria interface and its relevance for cell function remains elusive. We show by electron tomography that ER and mitochondria are adjoined by tethers that are approximately 10 nm at the smooth ER and approximately 25 nm at the rough ER. Limited proteolysis separates ER from mitochondria, whereas expression of a short "synthetic linker" (<5 nm) leads to tightening of the associations. Although normal connections are necessary and sufficient for proper propagation of ER-derived calcium signals to the mitochondria, tightened connections, synthetic or naturally observed under apoptosis-inducing conditions, make mitochondria prone to Ca2+ overloading and ensuing permeability transition. These results reveal an unexpected dependence of cell function and survival on the maintenance of proper spacing between the ER and mitochondria.
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