Gompertzian Mortality Originates in the Winding-down of the Mitotic Clock

Gompertzʹ age-related exponential increase in mortality rate and the abdurately flat mortality trajectory ofDrosophilaare paradoxical notions for metazoan aging theory. A multiclonal model of Gompertzian organisms provides a resolution by assuming that (a) conception initiated a stochastic process producing a train of replications of fixed length (the Hayflick limit); (b) unique stem cells arise early on to generate multiple vital clones; (c) life continues until one such clone critically depletes its replicative potential. Lifespan is thus governed by the time it takes to reach the terminal branches of the mitotic tree. Although these times are not independent,asymptoticindependence can be justified. This clears the way for asymptotic extreme-value theory to guarantee: (1) a non-increasing failure rate, under unlimited replicability; (2) an exponentially increasing failure rate, under limited replicability. However, to obtain an exact fit to the human force-of mortality function also requires the inclusion of the phenomenon of mitotic deceleration (implemented with a lognormal model of replication). Conclusion: thesine qua nonof Gompertzian mortality is cellular aging, expressed through these two mitotic phenomena. Conversely, those metazoa with unlimited cellular replicability, by staving off clonal failure would succumb only to catastrophic, age-independent events, yielding a constant mortality rate, the signature of a mitotic clock that does not run down.