Fussy mitochondria fuse in response to stress

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.