Replication, Parasite Control, and Energy Metabolism in Autocatalytic RNA Systems: A Minimal Computational Model

Abstract Self-sustained proto-Darwinian replication in an RNA world requires mechanisms to control molecular parasitism while sustaining the energetic demands of replication. How minimal RNA systems could coordinate replication, energy metabolism, and regulation remains an open question in origin-of-life research. Here, we develop a mathematical model of an autocatalytic ribozyme network integrating template-directed replication, an ATP/ADP energy cycle, and ATP-dependent allosteric regulation. In the absence of regulation, replication-error-derived parasites exploit the replicase and can destabilize or collapse the network. We show that allosteric interactions involving ATP-bound parasitic ribozymes and hyperparasites—parasites of parasites—can establish regulatory control and stabilize the system. Hyperparasites interact with the replicase and both ATP-bound and ATP-free parasitic ribozymes, but their sequestration of ATP imposes energetic constraints on replication. Increasing ATP turnover can alleviate these constraints, revealing a fundamental trade-off between parasite suppression and energy availability. Regulatory control can arise through two distinct mechanisms: intrinsically allostery-prone parasitic RNAs or trans-acting “allosterase” parasites that confer allosteric regulation on other RNAs. Once regulatory stability is established, catalytic ATP synthase/ATPase ribozymes can enhance ATP/ADP cycling, increasing energetic capacity and adaptability. These findings suggest a plausible evolutionary sequence in which parasite-mediated regulation precedes energetic optimization. More broadly, our model illustrates how molecular parasitism, rather than merely threatening early replicating systems, could contribute to the emergence of regulatory organization and increasingly autonomous proto-metabolic networks.