Two stochastic processes shape diverse senescence patterns in a single-cell organism

Abstract

Despite advances in aging research, a multitude of aging models, and empirical evidence for diverse senescence patterns, understanding is lacking of the biological processes that shape senescence, both for simple and complex organisms. We show that for a isogenic Escherichia coli bacterial population senescence results from two stochastic processes. A primary random deterioration process within the cell, such as generated by random accumulation of damage, leads to an exponential increase in mortality early in life followed by a late age mortality plateau; a secondary process of stochastic asymmetric transmission of an unknown factor at cell fission influences mortality. This second process is required to explain the difference between the classical mortality plateaus detected for young mothers offspring and the near non-senescence of old mothers offspring as well as the lack of a mother offspring correlation in age at death. We observed that life span is predominantly determined by underlying stochastic stage dynamics. Our findings support models based on stage-specific actions of alleles for the evolution of senescence. This support might be surprising since these models that have not specifically been developed in the context of simple, single cell organisms. We call for exploration of similar stochastic influences beyond simple organisms.