Nunes Palmeira, Raquel; (2024) Modelling the origin of heredity in protocells. Doctoral thesis (Ph.D), UCL (University College London).

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Abstract

The origin of life field is deeply divided into “metabolism first” and “genes first”. This dichotomy means few explored questions that arise from integrating metabolism and information: In what metabolic context could information evolve? What functions were first encoded? What conditions favoured selection in protocells? This thesis contributes to answering these questions. Firstly, I review the context and assumptions behind the main models of the origin of heredity. I highlight that gene-level selection gives rise to many theoretical obstacles to the evolution of complexity and point to Woese’s alternative hypothesis of “statistical proteins” in protocells as an overlooked possibility for the origin of heredity. Secondly, I present a protocell model with a simple metabolic network reflecting the core of conserved metabolism. I identified that nucleotide catalysis only supports growth when nucleotides directly catalyse CO2 fixation. Strong nucleotide catalysis of other pathways unbalances metabolism and slows protocell growth. Further, nucleotide autocatalysis alone leads to the accumulation of nucleotides at the expense of protocell growth. Thirdly, I present a model for the evolution of protocells containing RNA that is translated based on hydrophobicity. I show that polymerisation of random RNA in these protocells can lead to evolution towards optimum sequences. Selection is more effective at low probabilities of free polymerisation, as this introduces less noise; and maintaining two sequences only possible if the sequence encoding catalysis of carbon fixation is more easily synthesised at random than the sequence encoding catalysis of information functions. The same model is used to investigate the effect of translation and copying errors. I demonstrate that copying error has a stronger effect on protocell evolution, but translational errors surprisingly self-amplify. Further, I test the hypothesis that ribozyme catalysis of translation would be beneficial due to robustness to translational error, but simulation results show no support for this hypothesis.

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