Evolution of asymmetric division: an in-silico model
by
Armin Rashidi
Institute for Ageing and Health, Newcastle University, UK
Coauthors: Daryl Shanley

Symmetric reproduction precludes ageing; all individuals would be affected by any deterioration and the lineage would vanish. Segregation of damaged macromolecules, by asymmetric division, to one progeny cell results in an ageing parent and a rejuvenated daughter. Asymmetric reproduction is also a precursor for germ-soma specialization, a prerequisite for the evolution of multicellularity. However, surprisingly little work has been done on the evolution of asymmetry. Using in-silico experiments, we here determine circumstances under which selection forces drive the evolution of asymmetry. Assumptions used in the model are: (i) Limited resource availability creates a trade-off between investment in growth/reproduction and in maintenance/repair. (ii) The population is near its carrying capacity and the optimum investment strategy has already evolved. (iii) The rate of damage accumulation (r) is inversely related to the level of investment in maintenance/repair (m). (iv) The doubling time (T) is shortened by larger reproductive investments (b). (v) The likelihood of survival up to a certain time decreases with the time-integrated damage up to that time. (vi) The mode of damage distribution at division is an evolvable trait. The damage segregation coefficient, s, was allowed to evolve between zero (full symmetry) and one (full asymmetry), and was averaged over the population at any given time. The outcome of each run was defined as (a) asymmetry: s > 0.8 (more than 90% of damage segregating to one progeny cell) for at least 50% of the monitoring period or (b) symmetry: s > 0.8 for less than 25% of the monitoring period. Two stochastic parameters (random mutations and the likelihood of survival to next division) and three fundamental constants (T, C1, C2) are potential determinants of the dynamics of the system. C1 determines the shape of the relationship between r and T (and also the one between m and b if r and T are assumed linear functions of m and b, respectively), and C2 is the level of time-integrated damage above which the chance of survival is negligible. For a given T, the selection pressure for asymmetry is lower for more concave m/b trade-offs and and larger C2 values. Asymmetry evolves if damage-related mortality makes survival to the age at reproduction sufficiently unlikely. Of particular note, convex m/b trade-offs promote the evolution of asymmetry. These results have important implications to the evolution of multicellularity, ageing, and division of labour.

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Date received: May 12, 2008