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Quintana, A. et al.

Quintana, Schwarz, Schwindling, Lipp, Kaestner, Hoth,

Sustained Activity of Calcium Release-activated Calcium Channels Requires Translocation of Mitochondria to the Plasma Membrane.

A rise of the intracellular Ca(2+) concentration has multiple signaling functions. Sustained Ca(2+) influx across plasma membrane through calcium release-activated calcium (CRAC) channels is required for T-cell development in the thymus, gene transcription, and proliferation and differentiation of na??ve T-cells into armed effectors cells. Intracellular Ca(2+) signals are shaped by mitochondria, which function as a highly dynamic Ca(2+) buffer. However, the precise role of mitochondria for Ca(2+)-dependent T-cell activation is unknown. Here we have shown that mitochondria are translocated to the plasma membrane as a consequence of Ca(2+) influx and that this directed movement is essential to sustain Ca(2+) influx through CRAC channels. The decreased distance between mitochondria and the plasma membrane enabled mitochondria to take up large amounts of inflowing Ca(2+) at the plasma membrane, thereby preventing Ca(2+)-dependent inactivation of CRAC channels and sustaining Ca(2+) signals. Inhibition of kinesin-dependent mitochondrial movement along microtubules abolished mitochondrial translocation and reduced sustained Ca(2+) signals. Our results show how a directed movement of mitochondria is used to control important cellular functions such as Ca(2+)-dependent T-cell activation.[1]

References

Sustained Activity of Calcium Release-activated Calcium Channels Requires Translocation of Mitochondria to the Plasma Membrane. Quintana, A., Schwarz, E.C., Schwindling, C., Lipp, P., Kaestner, L., Hoth, M. J. Biol. Chem. (2006) [Pubmed]

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