No abstract

All life forms on earth ultimately descended from a primordial population dubbed the last universal common ancestor or LUCA via Darwinian evolution. Extant living systems share two salient functional features, a metabolism extracting and transforming energy required for survival, and an evolvable, informational polymer–the genome–conferring heredity. Genome replication invariably generates essential and ubiquitous genetic parasites. Here we model the energetic, replicative conditions of LUCA-like organisms and their parasites, as well as adaptive problem solving of host-parasite pairs. We show using an adapted Lotka-Volterra frame-work that three host-parasite pairs–individually a unit of a host and a parasite that is itself parasitized, therefore a nested parasite pair–are sufficient for robust and stable homeostasis, forming a life cycle. This nested parasitism model includes competition and habitat restriction. Its catalytic life cycle efficiently captures, channels and transforms energy, enabling dynamic host survival and adaptation. We propose a Malthusian fitness model for a quasispecies evolving through a host-nested parasite life cycle with two core features, rapid replacement of degenerate parasites and increasing evolutionary stability of host-nested parasite units from one to three pairs.

Autocatalytic networks likely played a central role in the shift from inanimate systems to protocells. Using an established hyperparasite framework, we model the emergence of antiparasite immunity using the Lotka Volterra equations. It builds on autocatalytic, increasingly complexed RNA networks reflecting the historical exposure to ubiquitous molecular parasites. First, upon parasite encounter, specific catalysts providing parasite resistance appear in primordial autocatalytic cycles, supplanted by promiscuous, efficiently self-replicating, but parasite sensitive ribozymes. This is supported by catalyst tradeoff analysis. Substrate promiscuity confers high catalytic activity, but entails parasite exposure, higher substrate specificity implies relatively lower activity, yet it offers parasite resistance. Second, sustained parasite influx generates hyperparasite cycles, reactivating the original, parasite-specific catalyst-subunit that now once more provides parasite resistance, in a homeostatically stabilized habitat, empirically consistent with phage satellites and defective RNA viruses induced across a range of parasite loads. Third, under continuous exposure to progressively elaborate parasite populations, hyperparasites degenerate and embody antiparasite immunity. Again, the observed triggering of antiviral immunity by phage satellite encoded antiphage systems and defective RNA virus genomes are in agreement with this model. As such, it offers an attractive and unifying theory for the spontaneous birth of immunity in early life.

No abstract

No abstract