It has been shown that apoptotic stimuli in yeast generate ROS that are closely correlated with the onset or progression of PCD (71) . We saw that, also the degree of rRNA decay corresponded to the cellular level of ROS, which was modified by using ROS scavenger (ascorbic acid) or ectopic expression of pro-or anti-apoptotic proteins (Bax and Bcl-x L , respectively) known to affect ROS generation. Also, rRNA degradation was more robust in oxidative stress defence mutants, both enzymatic and non-enzymatic, where intracellular ROS is not properly neutralized. All these observations argue that there is a direct link between ROS production and rRNA fragmentation. It can be envisaged that various reactive species themselves are able to produce endonucleolytic nicks in RNA molecules that will lead to breakdown, particularly as all mapped cleavages occur in singlestranded regions that constitute loops and bulges and are more accessible to chemical compounds in the solvent. However, this is not the case, given that specific RNA fragmentation did not occur in cells fixed with formaldehyde or ethanol prior to treatment with H 2 O 2 . In addition, oxidative agents used in this work generate different forms of ROS such as H 2 O 2 , hydroperoxide (LoaOOH, CHP and t-BHP), superoxide anion (menadione and paraquat) and hydroxyl free radical (produced from H 2 O 2 or superoxide anion). Although all were applied at toxic doses, only two of them, H 2 O 2 and menadione, mediated rRNA degradation, supporting the notion that oxidative compounds as such do not provoke cuts in RNA molecules within the cell. Taken together, this strongly suggests that active cellular machinery, such as signalling factors and RNA degrading enzyme(s), is required for this process. Nevertheless, these enzymatic activities are still to be identified. The closest yeast homologue of mammalian RNase L, Ire1, a sensor of the unfolded protein response, functions in the unconventional splicing of Hac1 pre-mRNA and contains protein kinase and endoribonuclease domains similar to those in RNase L (72) . Although our unpublished data show that deletion of Ire1 has no effect on the H 2 O 2 -induced rRNA degradation (M.S. and J.K.), it does not exclude its participation in other apoptotic pathways, for example those related to endoplasmic reticulum stress and unfolded protein response. We are currently testing several known yeast endo-an exonucleases for participation in apoptosis-related rRNA degradation. Preliminary observations suggest that, contrary to expectations, this function may involve not one but a number of unspecific nucleases, including mitochondrial Nuc1p, that act in a redundant fashion (M.S. and J.K., unpublished data).