The correlation between mitochondria and rRNA stability was assessed, in the first place, by checking rRNA level in respiratory-deficient rho0 cells lacking mtDNA in conditions inducing apoptosis, i.e. exposed to H 2 O 2 ( Figure 7A ), 175 mM acetic acid ( Figure 7B ), hyperosmotic stress (60% glucose, Figure 7C ) and during chronological ageing ( Figure 7D ). All treatments resulted in a remarkably robust degradation of the 25S and 5.8S rRNAs in rho0 strains when compared to the parental W303 and BY4741 strains (Figure 7 , Supplementary Figure S1E ; and data not shown). This points to the importance of the functioning mitochondria in the stressinduced rRNA degradation. To test the contribution of the oxidative phosphorylation, two mutants in these pathways were used, op1 with a point mutation in a major ADP/ATP carrier AAC2 (Arg96!His96), and a triple aac1/2/3Á deletion mutant (61) ( Figure 7E ). Both mutants behaved in a similar manner as rho0 cells and exhibited more pronounced rRNA degradation in the presence of H 2 O 2 than the isogenic wild-type; however, the phenotype was stronger for op1 than upon deletion of the three carrier proteins, possibly due to a dominant negative effect in the point mutant. In addition, treatment with F 0 -F 1 ATPase proton-pump inhibitors, oligomycin A (7.5 mg/ml) and sodium azide (NaN 3 , 1.5 mM) that block electron transfer and the synthesis of mitochondrial ATP (62-64), resulted in a moderate increase in the rRNA cleavage ( Figure 7F and Supplementary Figure S1D ). All these experiments indicate that the process of respiration, though generating the endogenous ROS, is also vital for counteracting its adverse effects. This was further supported by the degree of rRNA protection against oxidative damage caused by H 2 O 2 observed for yeast cells grown on different carbon sources, which are known to affect the level of respiration (65) . The most extensive RNA decay was observed in glucose, where a process called glucose repression discourages respiration. It was less pronounced in galactose and least of all in the nonfermentable source, glycerol, where mitochondrial respiration is forced ( Figure 7G) . These experiments directly correlate functional mitochondria and the process of respiration with the defence against oxidative stress triggered by H 2 O 2 , acetic acid, hyperosmosis and ageing that, among others, prevents destruction of cellular components, including rRNA.