As the oxidative stress in yeast proceeds through multiple pathways that involve different response mechanisms (1,2), we tested several known enzymes and factors that regulate these responses. These included two major transcription factors, Yap1 and Skn7, that control expression of several genes induced by oxidative stress and in this way participate in ROS sensing (1, 26, (49) (50) (51) , as well as components of antioxidant pathways, e.g. superoxide dismutases Sod1-2, glutathione peroxidases Gpx1-3, glutaredoxins Grx1-2, peroxiredoxins Tsa1-2, Prx1, Dot5 and Ahp1, thioredoxins Trx1-2 and thioredoxin reductases Trr1-2 (24,52). These enzymes are required for protection against ROS either by catalysing the breakdown of oxidative compounds or by restoring natural intracellular redox equilibrium. In addition, as glutathion protects cells against ROS, we also used a gsh1D strain lacking a g-glutamylcysteine synthetase, which, when grown on glutathion-free synthetic medium, leads to glutathion depletion and cell death (36, 53) . Strains lacking these proteins are more sensitive to several oxidants than their isogenic wild-types (2), and following treatment with H 2 O 2 they showed a marked increase in the 25S rRNA degradation, however, to different degrees depending on the mutant. In Figure 5B -D, yap1D, skn7D, gpx1/2/3D, sod1/2D, grx1/2-D, prxD (tsa1/2D/prx1D/ ahp1D/dot5D) and gsh1D strains are shown, which gave the most evident effects in comparison with their respective isogenic wild-types, particularly when considering the decay rate of the mature 25S rRNA. These data indicate that properly functioning oxidative stress response also protects cellular components such as nucleic acids from the attack by ROS and that defects at any step of this defence result in a more severe and faster breakdown. It is noteworthy that multiple anti-oxidant mutants lacking all components of each enzymatic pathway exhibit a stronger effect on the 25S degradation than single mutants, pointing to the additive protection actions of these systems. Striking effects on rRNA stability in strains lacking stress response transcription factors Yap1 and Skn7 indicate that the synthesis of new anti-oxidant proteins that are induced by oxidative stress might be required for protection of ribosomes. Consistently, blocking protein synthesis by pre-treatment with cycloheximide resulted in somehow stronger rRNA degradation (Supplementary Figure S1A, lanes 1-5 and 11-15 ).