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Two stochastic processes shape diverse senescence patterns in a single‐cell organism
Author(s) -
Steiner Ulrich K.,
Lenart Adam,
Ni Ming,
Chen Peipei,
Song Xiaohu,
Taddei François,
Vaupel James W.,
Lindner Ariel B.
Publication year - 2019
Publication title -
evolution
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.84
H-Index - 199
eISSN - 1558-5646
pISSN - 0014-3820
DOI - 10.1111/evo.13708
Subject(s) - biology , senescence , offspring , evolutionary biology , organism , longevity , stochastic process , population , genetics , demography , statistics , pregnancy , mathematics , sociology
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.