Control of mitochondrial motility and distribution by the calcium signal

Mitochondria are dynamic organelles in cells. The control of mitochondrial motility by signaling mechanisms and the significance of rapid changes in motility remains elusive. In cardiac myoblasts, mitochondria were observed close to the microtubular array and displayed both short- and long-range movements along microtubules. By clamping cytoplasmic Ca2+ (Ca2+c) at various levels, mitochondrial motility was found to be regulated by Ca2+ in the physiological range. Maximal movement was obtained at resting Ca2+c with complete arrest at 1-2 microM. Movement was fully recovered by returning to resting Ca2+c, and inhibition could be repeated with no apparent desensitization. The inositol 1,4,5-trisphosphate- or ryanodine receptor-mediated Ca2+c signal also induced a decrease in mitochondrial motility. This decrease followed the spatial and temporal pattern of the Ca2+c signal. Diminished mitochondrial motility in the region of the Ca2+c rise promotes recruitment of mitochondria to enhance local Ca2+ buffering and energy supply. This mechanism may provide a novel homeostatic circuit in calcium signaling.