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Fig. 1 | BMC Bioinformatics

Fig. 1

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

Fig. 1

a Illustration of the model. The cell grows until it reaches a critical volume and divides. It accumulates damage over time, which slows down volume growth. The accumulated damage can also be repaired. There is no separate mechanism for killing a cell due to damage, because high level of accumulated damage will prevent a cell from dividing and cause it to be rapidly overtaken by faster-dividing cells. b The cell volume module of the model. The volume grows exponentially until it reaches a generation-dependent critical volume and the cell divides (blue dashed line). c Two mechanisms of particular interest in this study: segregation of damaged proteins in mother cells, and division asymmetry of cell volume. Yellow dots indicate normal proteins, while green dots indicate damaged proteins. d Illustration of the exponential growth of simulated cell population. An initial population of 2000 cells were simulated for 6000 min with periodic resampling (blue dashes) every time the population size exceeds 2 million cells. The red dashed line indicates the expected population size without sampling

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