Ten years ago the genes and pathways that regulate the chronological life span of eukaryotes were unknown. Since then, studies mostly performed in S. cerevisiae, C. elegans, Drosophila, and mice have resulted in the identification of many genes and a few conserved pathways that can be activated or inactivated to extend the life span of the organism. These pathways also regulate stress resistance, the storage of reserve carbon sources, and entry into hypometabolic starvation response phases.
Worms, flies and mice are excellent model systems to study aging because of their progressively closer relationship to humans. By contrast, the unicellular S. cerevisiae is a valuable model system because it is very simple and amenable to powerful techniques and technologies such as transposon mutagenesis and high-density oligonucleotide genome-wide arrays of tagged deletion mutations. The information on the function or putative function of the majority of S. cerevisiae proteins contributes further to making this unicellular eukaryote one of the simplest and most valuable model systems to study the fundamental mechanisms of aging. Whereas aging in S. cerevisiae has been studied for 50 years by measuring the number of buds generated by an individual mother cell, studies of the chronological life span of yeast populations have been mostly published in the past 10 years. These studies have indicated that yeast and higher eukaryotes use similar ''molecular strategies'' to regulate entry into maintenance phases that extend life span. These strategies, which include down-regulation of glucose- or IGF-I-like receptor activated signal trans-duction proteins, up-regulation of antioxidant enzymes and heat shock proteins, and increased storage of reserve nutrients, are likely to also extend to many additional biological processes including repair and replacement systems. We predict that we will continue to observe many similarities and some differences between the genes and pathways that regulate aging and life span in yeast and higher eukaryotes. An important aim should be to determine whether the knowledge of these conserved ''antiaging'' pathways can be applied to the development of drugs that cause a switch to an antidisease mode in humans. Whereas modern medicine is focused on the treatment of diseases, the identification of Methuselah genes could ignite a novel ''evolutionary medicine'' approach in which multiple diseases of aging including cancer, Alzheimer's, and cardiovascular diseases are prevented pharmacologically.
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