Mitochondrial respiration protects rRNA against deleterious consequences of ROS Certain aspects of apoptosis, such as the change in mitochondrial membrane potential, fragmentation of mitochondria and the requirement of cyt c and AIF release to the cytoplasm, are strongly conserved among different organisms and point to the pivotal role of mitochondria. In yeast, PCD pathways triggered by acetic acid, Bax expression and pheromone, are strictly correlated with these events and do not proceed in cells devoid of mtDNA (rho0) (31, 60) . During chronological ageing and hyperosmotic shock, rho0 strains were reported to have somehow higher survival, which can be attributed to their long doubling time (1.5 to 2-fold), but they still die apoptotically (23, 73) . However, mitochondrial function is required for resistance to oxidative stress by way of detoxification or repair of the oxidative damage and, consequently, rho0 cells are more sensitive to several oxidants, have higher level of endogenous ROS and undergo apoptosis caused by H 2 O 2 or amino-acid starvation (61, 71, (74) (75) (76) (77) . Also, mammalian rho0 cell lines undergo apoptosis in response to some but not all cell death-activating stimuli. It has been postulated that these differences may arise from a distinct mechanism by which rho0 cells maintain membrane potential by way of ATP consumption (78) .