title: Programmed death in yeast as adaptation?
abstract: During recent years, several pieces of indirect evidence of a programmed death in yeast have been published. Among them there are observations that some mammalian pro- or anti-apoptotic proteins induce or prevent the death of yeast; some toxic compounds kill yeast at lower concentrations if protein synthesis is operative; this death, as well as the death due to certain mutations, shows some apoptotic markers. In April 2002, the yeast programmed death concept received direct support. Madeo et al. [Madeo et al., Mol. Cell 9 (2002) 911-917] disclosed a caspase which is activated by H(2)O(2) or aging and is required for the protein-synthesis-dependent death of yeast. Thus, a specific apoptosis-mediating protein was identified for the first time in Saccharomyces cerevisiae. Independently, Severin and Hyman [Severin, F.F., Hyman, A.A., Curr. Biol. 12 (2002) R233-R235] discovered that death of yeast, induced by a high level of a pheromone, is programmed. In particular, the death was found to be prevented by cycloheximide and cyclosporin A. It required mitochondrial DNA, cytochrome c and the pheromone-initiated protein kinase cascade. When haploids of opposite mating types were mixed, some cells died, the inhibitory pattern being the same as in the case of the killing by pheromone. Inhibition of mating proved to be favorable for death. Thus, pheromone not only activates mating but also eliminates yeast cells failing to mate. Such an effect should (i) stimulate switch of the yeast population from vegetative to sexual reproduction, and (ii) shorten the life span and, hence, accelerate changing of generations. As a result, the probability of appearance of new traits could be enhanced when ambient conditions turned for the worse.
authors.affiliation: Belozersky Institute of Physico-Chemical Biology, Moscow State University, Russia. skulach@belozersky.msu.ru
authors.forename: Vladimir P
authors.initials: VP
authors.lastname: Skulachev
mesh_terms: D000222:Adaptation, Physiological; D017209:Apoptosis / Q000502:physiology*; D020169:Caspases / Q000502:physiology; D003513:Cycloheximide / Q000494:pharmacology; D016572:Cyclosporine / Q000494:pharmacology; D000072235:Mating Factor; D008928:Mitochondria / Q000502:physiology; D008954:Models, Biological; D010455:Peptides / Q000502:physiology; D010675:Pheromones / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D012441:Saccharomyces cerevisiae / Q000166:cytology* / Q000187:drug effects / Q000502:physiology*; D029701:Saccharomyces cerevisiae Proteins / Q000502:physiology
chemical_list: D010455:Peptides; D010675:Pheromones; D017382:Reactive Oxygen Species; D029701:Saccharomyces cerevisiae Proteins; D000072235:Mating Factor; D016572:Cyclosporine; D003513:Cycloheximide; D020169:Caspases