Degradation of the 25S/5.8S rRNAs is observed in all conditions inducing apoptosis, however, this process is not dependent on Yca1 and Aif1. On the other hand, mutations in histone H2B that inhibit phosphorylation at Ser10 and block the progress of H 2 O 2 -induced apoptosis also severely affect rRNA degradation. More importantly, rRNA degradation coincides with apoptotic DNA fragmentation; from several compounds that lead to oxidative stress and cell death, only those that provoked DNA destruction also triggered rRNA decay. Furthermore, at least some apoptotic pathways strictly require the involvement of mitochondria and do not occur in yeast lacking mtDNA, whereas rRNA degradation in all stress conditions tested is more powerful in rho0 cells. To sum up: rRNA decay induced by apoptotic stimuli occurs during cell death pathway that involves ROS generation, mitochondrial activity, fragmentation of chromosomes and histone modification but not apoptotic regulators, Yca1 and Aif1. This could be due to the existence of numerous different but partly overlapping PCD mechanisms, whether caspase-and mitochondria-dependent or independent. Ever increasing numbers of such pathways has been described in the literature in recent years. However, we favour a different model, where all these elements function in concert at different steps of the whole scenario. Stress stimuli induce signals, possibly via ROS, affecting different levels of gene expression, namely chromatin modifications, transcription and translation, which as a result activate defence response. At this level, mitochondrial respiration helps to protect cellular components via adaptive mechanisms with anti-oxidant functions. Even so, when the attack is not successfully pacified, generated ROS molecules initiate the destruction of cellular machineries, targeting in the first place crucial elements such as protein synthesis (i.e. ribosomes). Now, the progression of the response comes to the crossroadsif the conditions are appropriate, the cascade of events leading to apoptosis is triggered (e.g. release of CytC and other mitochondrial factors to the cytoplasm) resulting in cell death with characteristic apoptotic markers. Alternatively, when apoptotic prerequisites are not met, cells do not enter this pathway. The more fit cells escape death, whereas others die anyway, maybe less rapidly and through a different pathway. In this scenario, certain events, including generation of ROS, histone modifications and possibly also RNA fragmentation, occur upstream of subsequent steps, such as activation of caspases and other apoptotic regulators with resulting apoptotic phenotypes. Virus Adaptation by Manipulation of Host's Gene Expression Viruses adapt to their hosts by evading defense mechanisms and taking over cellular metabolism for their own benefit. Alterations in cell metabolism as well as side-effects of antiviral responses contribute to symptoms development and virulence. Sometimes, a virus may spill over from its usual host species into a novel one, where usually will fail to successfully infect and further transmit to new host. However, in some cases, the virus transmits and persists after fixing beneficial mutations that allow for a better exploitation of the new host. This situation would represent a case for a new emerging virus. Here we report results from an evolution experiment in which a plant virus was allowed to infect and evolve on a naïve host. After 17 serial passages, the viral genome has accumulated only five changes, three of which were non-synonymous. An amino acid substitution in the viral VPg protein was responsible for the appearance of symptoms, whereas one substitution in the viral P3 protein the epistatically contributed to exacerbate severity. DNA microarray analyses show that the evolved and ancestral viruses affect the global patterns of host gene expression in radically different ways. A major difference is that genes involved in stress and pathogen response are not activated upon infection with the evolved virus, suggesting that selection has favored viral strategies to escape from host defenses. One of the first consequences of organisms' adaptation to new environments is the manipulation of resources [1] [2] [3] [4] . In this sense, the interaction between intracellular parasites and their hosts represents a paradigm of resource manipulation. In general, a virulent relationship results in the alteration of many aspects of cellular metabolism and development, which are taken over in the parasite's own benefit [5] [6] [7] . Whether the relationship between a host and a parasite evolves towards a more or less virulent or benign situation depends on several genetic and ecological factors that may affect virus accumulation and transmission between hosts [5] . Of particular interest in the context of emerging infectious diseases is the characterization of changes in the pathogen's genome that are responsible for adaptation to a new host after spilling over from the original one and to understand how these changes may alter host's metabolic and regulatory interactions.