Role of cardiolipin on tBid and tBid/Bax synergistic effects on yeast mitochondria.

Cell Death Differ

Institut Cochin, Team 'Cancer, Apoptosis and Mitochondria', CNRS UMR 8104/INSERM U567/Université ParisV, R. Descartes--24 rue du Faubourg Saint-Jacques, Paris, France.

Published: June 2005

The apoptotic effector Bid regulates cell death at the level of mitochondria. Under its native state, Bid is a soluble cytosolic protein that undergoes proteolysis and yields a 15 kDa-activated form tBid (truncated Bid). tBid translocates to mitochondria and participates in cytochrome c efflux by a still unclear mechanism, some of them at least mediated by Bax. Using mitochondria isolated from wild-type and cardiolipin (CL)-synthase-less yeast strains, we observed that tBid perturbs mitochondrial bioenergetics by inhibiting state-3 respiration and ATP synthesis and that this effect was strictly dependent on the presence of CL. In a second set of experiments, heterologous coexpression of tBid and Bax in wild-type and CL-less yeast strains showed that (i) tBid binding and the subsequent alteration of mitochondrial bioenergetics increased Bax-induced cytochrome c release and (ii) the absence of CL favors Bax effects independently of the presence of t-Bid. These data support recent views suggesting a dual function of CL in mitochondria-dependent apoptosis.

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http://dx.doi.org/10.1038/sj.cdd.4401585DOI Listing

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