The coexistence of catalytic replicators

(information-carrying molecules with enzymatic activities) in the Hipercycle (Eigen and Schuster, 1971; Boerlijst and Hogeweg, 1991) or in the Metabolic replicator model (Czárán and Szathmáry, selleck compound 2000; Könnyü et al.) is unthinkable without previous specialization processes leading to some kind of “enzyme click here specificity”. The common assumption of these models is that every replicator type has a well-defined, specific function with which it contributes to the maintenance of the system. Thus, if any one of the cooperating replicator types is absent, the replicator community as a whole collapses due to the missing function. Both the Hypercycle and the Metabolic Replicator models are concerned with the problem of the coexistence of specialized replicators and their resistance to the attack of parasitic replicators which do not contribute to the common good at all, or even do explicit harm to the system. These models do not explain, however, why and how specialization comes about in a system of catalytic replicators.

That is what we attempt in our present work. This model is based on the Metabolic replicator system in which each replicator type is supposed to catalyze a specific reaction of a simple network of metabolism. Metabolism produces the monomers for the replication of all the replicators, thus it is necessary that the reactions of metabolism be catalyzed, otherwise the system dies out. To keep the system at its simplest form, we assume that the metabolic “network” is constituted by two chemical reactions (reaction A and B), and that the replicators can catalyze both these reactions at the beginning,

NU7441 in vitro i.e., the initial replicator population is that of “generalists”. We also assume a trade-off relation between the two different enzymatic activities: a good catalyst of reaction A cannot be very good at catalyzing reaction B, and vice versa. Another trade-off is assumed between enzymatic activity and replication rate: good enzymes cannot replicate very fast, selleck products and fast replicators cannot be good catalysts. Of course, fast and non-catalyzing replicators are the parasites of this system. We let the system of different generalists evolve on a two-dimensional cellular automaton, assuming that mutations (constrained by the unified trade-off function) can occur during replications. We search for parts of the parameter space of the model that allow for specialization (extreme evolutionary shift towards a mix of the two specialist types of replicators) and parasite resistance. We find that under certain conditions (i.e., at limited mobility of the replicators on the mineral surface, and for certain shapes and parameter regimes of the trade-off function) specialization and parasite resistance both occur in the metabolic system. Boerlijst, M. C. and Hogeweg, P. (1991). Spiral wave structure in pre-biotic evolution: hypercycles stable against parasites. Physica D 48:17–28. Dieckmann, U., Law, R., and Metz, J. A. J.