Recent evidence suggests that cells employ functionally asymmetric partitioning schemes in division to cope with aging. We explore various schemes in silico, with a stochastic model of Escherichia coli that includes gene expression, non-functional proteins generation, aggregation and polar retention, and molecule partitioning in division. The model is implemented in SGNS2, which allows stochastic, multi-delayed reactions within hierarchical, transient, interlinked compartments. After setting parameter values of non-functional proteins' generation and effects that reproduce realistic intracellular and population dynamics, we investigate how the spatial organization of non-functional proteins affects mean division times of cell populations in lineages and, thus, mean cell numbers over time. We find that division times decrease for increasingly asymmetric partitioning. Also, increasing the clustering of non-functional proteins decreases division times. Increasing the bias in polar segregation further decreases division times, particularly if the bias favors the older pole and aggregates' polar retention is robust. Finally, we show that the non-energy consuming retention of inherited non-functional proteins at the older pole via nucleoid occlusion is a source of functional asymmetries and, thus, is advantageous. Our results suggest that the mechanisms of intracellular organization of non-functional proteins, including clustering and polar retention, affect the vitality of E. coli populations.
Keywords: In silico models; Non-functional proteins; division times; functional asymmetries; partitioning schemes.