Aging is typically accompanied by an exponentially increasing hazard rate of death – i.e. the probability that an individual within a population will die within a given time interval. Previous biochemical analyses of aging cells focused on cells aged for only ∼10 generations due to technical limitations [50]. At this age, a diploid cell population in the common laboratory S288C strain is still relatively young: It retains >95% viability and has yet to experience the dramatic increase in hazard rate of death that affects cells near their median RLS [16], [51]. Using the MEP, we developed an effective purification method to isolate age-matched populations near their median RLS which allowed us to make new observations that change our understanding of age-associated processes. Earlier reports concluded that fob1Δ effectively suppressed the accumulation of ERCs [32], [42]. By examining populations at their median life span we found that ERC levels in fob1Δ cells actually increase significantly as cells approach their median RLS, although their accumulation was reduced/delayed compared to wild type cells. The extension of our ability to observe age-associated genetic and
