We have studied the pathways for Ca2+ transport in mitochondria of the fruit fly Drosophila melanogaster. We demonstrate the presence of ruthenium red (RR)-sensitive Ca2+ uptake, of RR-insensitive Ca2+ release, and of Na+-stimulated Ca2+ release in energized mitochondria, which match well characterized Ca2+ transport pathways of mammalian mitochondria. Following larger matrix Ca2+ loading Drosophila mitochondria underwent spontaneous RR-insensitive Ca2+ release, an event that in mammals is due to opening of the permeability transition pore (PTP). Like the PTP of mammals, Drosophila Ca2+-induced Ca2+ release could be triggered by uncoupler, diamide, and N-ethylmaleimide, indicating the existence of regulatory voltage- and redox-sensitive sites and was inhibited by tetracaine. Unlike PTP-mediated Ca2+ release in mammals, however, it was (i) insensitive to cyclosporin A, ubiquinone 0, and ADP; (ii) inhibited by P(i), as is the PTP of yeast mitochondria; and (iii) not accompanied by matrix swelling and cytochrome c release even in KCl-based medium. We conclude that Drosophila mitochondria possess a selective Ca2+ release channel with features intermediate between the PTP of yeast and mammals.
Properties of Ca2+ Transport in Mitochondria of Drosophila melanogaster
VON STOCKUM, SOPHIA HILDE ELSE;BASSO, EMY;BERNARDI, PAOLO
2011
Abstract
We have studied the pathways for Ca2+ transport in mitochondria of the fruit fly Drosophila melanogaster. We demonstrate the presence of ruthenium red (RR)-sensitive Ca2+ uptake, of RR-insensitive Ca2+ release, and of Na+-stimulated Ca2+ release in energized mitochondria, which match well characterized Ca2+ transport pathways of mammalian mitochondria. Following larger matrix Ca2+ loading Drosophila mitochondria underwent spontaneous RR-insensitive Ca2+ release, an event that in mammals is due to opening of the permeability transition pore (PTP). Like the PTP of mammals, Drosophila Ca2+-induced Ca2+ release could be triggered by uncoupler, diamide, and N-ethylmaleimide, indicating the existence of regulatory voltage- and redox-sensitive sites and was inhibited by tetracaine. Unlike PTP-mediated Ca2+ release in mammals, however, it was (i) insensitive to cyclosporin A, ubiquinone 0, and ADP; (ii) inhibited by P(i), as is the PTP of yeast mitochondria; and (iii) not accompanied by matrix swelling and cytochrome c release even in KCl-based medium. We conclude that Drosophila mitochondria possess a selective Ca2+ release channel with features intermediate between the PTP of yeast and mammals.
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