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Stochastic modeling of aging cells reveals how damage accumulation, repair, and cell-division asymmetry affect clonal senescence and population fitness.

ABSTRACT: BACKGROUND:Asymmetry during cellular division, both in the uneven partitioning of damaged cellular components and of cell volume, is a cell biological phenomenon experienced by many unicellular organisms. Previous work based on a deterministic model claimed that such asymmetry in the partitioning of cell volume and of aging-associated damage confers a fitness benefit in avoiding clonal senescence, primarily by diversifying the cellular population. However, clonal populations of unicellular organisms are already naturally diversified due to the inherent stochasticity of biological processes. RESULTS:Applying a model of aging cells that accounts for natural cell-to-cell variations across a broad range of parameter values, here we show that the parameters directly controlling the accumulation and repair of damage are the most important factors affecting fitness and clonal senescence, while the effects of both segregation of damaged components and division asymmetry are frequently minimal and generally context-dependent. CONCLUSIONS:We conclude that damage segregation and division asymmetry, perhaps counterintuitively, are not necessarily beneficial from an evolutionary perspective.

SUBMITTER: Song R

PROVIDER: S-EPMC6631810 | biostudies-other | 2019 Jul

REPOSITORIES: biostudies-other

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Stochastic modeling of aging cells reveals how damage accumulation, repair, and cell-division asymmetry affect clonal senescence and population fitness.

Song Ruijie R Acar Murat M

BMC bioinformatics 20190715 1

<h4>Background</h4>Asymmetry during cellular division, both in the uneven partitioning of damaged cellular components and of cell volume, is a cell biological phenomenon experienced by many unicellular organisms. Previous work based on a deterministic model claimed that such asymmetry in the partitioning of cell volume and of aging-associated damage confers a fitness benefit in avoiding clonal senescence, primarily by diversifying the cellular population. However, clonal populations of unicellul ...[more]

PMID: 31307385

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Project description:The evolutionary theories of aging are useful for gaining insights into the complex mechanisms underlying senescence. Classical theories argue that high levels of extrinsic mortality should select for the evolution of shorter lifespans and earlier peak fertility. Non-classical theories, in contrast, posit that an increase in extrinsic mortality could select for the evolution of longer lifespans. Although numerous studies support the classical paradigm, recent data challenge classical predictions, finding that high extrinsic mortality can select for the evolution of longer lifespans. To further elucidate the role of extrinsic mortality in the evolution of aging, we implemented a stochastic, agent-based, computational model. We used a simulated annealing optimization approach to predict which model parameters predispose populations to evolve longer or shorter lifespans in response to increased levels of predation. We report that longer lifespans evolved in the presence of rising predation if the cost of mating is relatively high and if energy is available in excess. Conversely, we found that dramatically shorter lifespans evolved when mating costs were relatively low and food was relatively scarce. We also analyzed the effects of increased predation on various parameters related to density dependence and energy allocation. Longer and shorter lifespans were accompanied by increased and decreased investments of energy into somatic maintenance, respectively. Similarly, earlier and later maturation ages were accompanied by increased and decreased energetic investments into early fecundity, respectively. Higher predation significantly decreased the total population size, enlarged the shared resource pool, and redistributed energy reserves for mature individuals. These results both corroborate and refine classical predictions, demonstrating a population-level trade-off between longevity and fecundity and identifying conditions that produce both classical and non-classical lifespan effects.

Dataset Information

Stochastic modeling of aging cells reveals how damage accumulation, repair, and cell-division asymmetry affect clonal senescence and population fitness.

Publications

Stochastic modeling of aging cells reveals how damage accumulation, repair, and cell-division asymmetry affect clonal senescence and population fitness.

Similar Datasets

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