Before simulating the full life-cycle of a vesicular artificial cell, it is important to establish a model that allows vesicular cells to maintain their structure on the timescale of component turnover. Component turnover involves the continuous synthesis and destruction of cell components. This also requires a regulatory mechanism to ensure a stable-sized vesicular cell. In this section we demonstrate how vesicles composed of metabolizing components can achieve a stable size, for the two cases:
(i) purely molecular turnover and
(ii) loss of membrane components through budding and/or fission.
The basic mechanisms of steady state size depend on an effective combination of
processes dependent on the different regions defined by the presence of a vesicular membrane. The law of mass-action implies reactions proportional to local concentrations, but concentrations depend on the volume of the region in which the chemicals are free to move, and this is modulated by the presence of membrane barriers and by diffusion. For a vesicle of radius R, the
a) the interior of the vesicle: volume scales as R3
b) the membrane itself: surface scales as R2
c) exterior of the vesicle : diffusion limited (Schmoluchowski) rate scales as R.
Varela's original model of vesicular autopoeisis was stabilized by the finite number of catalysts within the vesicle (case a): the concentration scaling as 1/R3. We sought more stable mechanisms (in the presence of genetic replication). One key mechanism, also allowing the enrichment of metabolites within the cell was proposed by R. Serra et.al. We verified its efficacy in an mprDPD simulation of enrichment. This in turn is an alternative to the enrichment mechanisms based on asymmetric shaped pores investigated in morphological computation by Protolife.