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[摘要]：When cells become committed to apoptosis, they shatter their mitochondrial networks through the actions of the mitochondrial fission protein DRP1. Massive fragmentation of mitochondria facilitates simultaneous release of cytochrome c from all mitochondria within a cell, thus promoting further progression along the apoptotic pathway. In this issue, Tondera et al (2009) describe a new process with the opposite effect. When cells are subjected to modest levels of stress (well below levels needed to induce apoptosis), their mitochondria fuse to each other forming a closed network, similar to networks observed when mitochondrial fission is blocked. Stress-induced mitochondrial hyperfusion (SIMH), as this process was called, might counter stress by optimizing mitochondrial ATP production. |
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