Abstract
Calcium oscillations control mitochondrial motility along the microtubules and in turn, support on-demand distribution of mitochondria. However, the mechanism mediating the Ca(2+) effect remained a mystery. Recently, several papers reported on the Ca(2+)-dependent regulation of mitochondrial dynamics by a Miro-Milton complex linking mitochondria to kinesin motors. Both mitochondrial motility and fusion-fission dynamics seem to be sensitive to a Ca(2+)-dependent switch by this complex. Evidence is emerging that calcium signaling through Miro-Milton is central to coordination of the local oxidative metabolism with the energy demands and protection against Ca(2+)-induced cell injury.