Cellular longevity of budding yeast during replicative and chronological aging

Mechanisms of aging and its retardation are evolutionarily conserved from unicellular to multicellular organisms. Several laboratory models, including budding yeast, have contributed to a better understanding of the complexity of aging and longevity. Budding yeast gradually loses the ability of producing daughter cells in rich media, and then loses viability in exhausted media during the aging process. According to these distinguishable losses, there are two measurable lifespans in budding yeast: replicative life span (RLS) and chronological life span (CLS). These two types of lifespans share common longevity-regulating pathways, such as Target of Rapamycin (TOR) signaling, and have non-overlapping pathways between chronologically long-lived mutants and replicatively long-lived mutants. CLS and RLS can be extended through genetic mutation, caloric restriction, and chemical treatment (e.g., rapamycin). We reviewed methodological properties of CLS and RLS, and discussed genes related to these lifespans. Particularly, we focused on two genes, Sir2 and Tor1, in context of their association with replicative and chronological cellular aging. We also described novel genes and primary biological processes responsible for cellular longevity from genome-wide studies.