fig1

Figure 1. The evolution of somatic mutation rates suggests that cell health is amenable to engineering by exploiting mechanisms naturally present in long-lived species. (A) Cells gradually accumulate different types of molecular damage, including DNA mutations, as they progress through biological time, eventually resulting in old dysfunctional cells (red). Cagan et al. report differences in somatic mutation rates across species, suggesting that this damage is under evolutionary constraint^[5]. (B) This observation shows that this and potentially other age-related losses of function are in principle amenable to interventions that recapitulate the natural molecular processes in long-lived animals. Such interventions could program cell trajectories to either halt decline at a tolerable level (dark green cell) or reverse aging phenotypes (bright green cell).