Editors' ChoiceCell Biology

Mobile Energy Stations

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Science's STKE  30 Nov 2004:
Vol. 2004, Issue 261, pp. tw432
DOI: 10.1126/stke.2612004tw432

Mitochondria are mobile organelles, and the movement of these energy-producing organelles may redistribute the spatial pattern of ATP production and calcium buffering. Yi et al. found that the cytosolic calcium concentration ([Ca2+]c) controlled the rate of mitochondrial movement in H92c myoblasts. Using calcium-sensitive dyes and labeled mitochondria, the movement of mitochondria in response to various treatments that raise or lower [Ca2+]c was tested. Increases in ([Ca2+]c) produced a complete inhibition of mitochondrial motility. This inhibition of motility did not require calcium uptake into the mitochondria, because even cells treated with a mitochondrial uncoupler, which blocks calcium uptake and eliminates the mitochondrial membrane potential, showed a complete cessation of mitochondrial movement in response to elevations in [Ca2+]c. When the increase in [Ca2+]c was not uniform in the cell, movement was inhibited maximally in areas where the [Ca2+]c was highest. Although the mitochondria appeared to predominantly move along microtubules, the microtubule motors do not appear to have intrinsic calcium binding or sensitivity, and Yi et al. showed that neither inhibition of the Ca2+-calmodulin-dependent kinases nor inhibition of the phosphatase calcineurin prevented calcium-triggered cessation of mitochondrial movement. Remaining questions include the mechanism by which calcium affects mitochondrial motility and to what extent inhibition of motility contributes to mitochondrial calcium signaling.

M. Yi, D. Weaver, G. Hajnóczky, Control of mitochondrial motility and distribution by the calcium signal: a homeostatic circuit. J. Cell. Biol. 167, 661-672 (2004). [Abstract] [Full Text]

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