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

Despite advances in aging research, a multitude of aging models, and
empirical evidence for diverse senescence patterns, understanding of the
biological processes that shape senescence is lacking. We show that
senescence of an isogenic Escherichia coli bacterial population results
from two stochastic processes. The first process is a random deterioration
process within the cell, such as generated by random accumulation of
damage. This primary process leads to an exponential increase in mortality
early in life followed by a late age mortality plateau. The second process
relates to the stochastic asymmetric transmission at cell fission of an
unknown factor that influences mortality. This secondary process explains
the difference between the classical mortality plateaus detected for young
mothers’ offspring and the near nonsenescence of old mothers’ offspring as
well as the lack of a mother–offspring correlation in age at death. We
observed that lifespan is predominantly determined by underlying
stochastic stage dynamics. Surprisingly, our findings support models
developed for metazoans that base their arguments on stage‐specific
actions of alleles to understand the evolution of senescence. We call for
exploration of similar stochastic influences that shape aging patterns
beyond simple organisms.