Previously, life span extension by fob1Δ was interpreted as a result of reduced ERC accumulation to a degree at which RLS becomes limited by an alternative mechanism [32], [42]. However, we found that ERCs accumulate to high levels even in fob1Δ cells (Figure 8). This result could be interpreted in two ways that support opposing models for how life span is limited in fob1Δ cells. First, the delayed accumulation of ERCs early in life could extend, but still limit, RLS in fob1Δ cells. Alternatively, the life span-limiting function of ERCs may be Fob1-dependent, suggesting that RLS in fob1Δ cells is limited by an alternative mechanism.
