Dataset Information

Mathematical modeling reveals spontaneous emergence of self-replication in chemical reaction systems.

ABSTRACT: Explaining the origin of life requires us to elucidate how self-replication arises. To be specific, how can a self-replicating entity develop spontaneously from a chemical reaction system in which no reaction is self-replicating? Previously proposed mathematical models either supply an explicit framework for a minimal living system or consider only catalyzed reactions, and thus fail to provide a comprehensive theory. Here, we set up a general mathematical model for chemical reaction systems that properly accounts for energetics, kinetics, and the conservation law. We found that 1) some systems are collectively catalytic, a mode whereby reactants are transformed into end products with the assistance of intermediates (as in the citric acid cycle), whereas some others are self-replicating, that is, different parts replicate each other and the system self-replicates as a whole (as in the formose reaction, in which sugar is replicated from formaldehyde); 2) side reactions do not always inhibit such systems; 3) randomly chosen chemical universes (namely random artificial chemistries) often contain one or more such systems; 4) it is possible to construct a self-replicating system in which the entropy of some parts spontaneously decreases, in a manner similar to that discussed by Schrödinger; and 5) complex self-replicating molecules can emerge spontaneously and relatively easily from simple chemical reaction systems through a sequence of transitions. Together, these results start to explain the origins of prebiotic evolution.

SUBMITTER: Liu Y

PROVIDER: S-EPMC6295724 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature

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Mathematical modeling reveals spontaneous emergence of self-replication in chemical reaction systems.

Liu Yu Y Sumpter David J T DJT

The Journal of biological chemistry 20181003 49

Explaining the origin of life requires us to elucidate how self-replication arises. To be specific, how can a self-replicating entity develop spontaneously from a chemical reaction system in which no reaction is self-replicating? Previously proposed mathematical models either supply an explicit framework for a minimal living system or consider only catalyzed reactions, and thus fail to provide a comprehensive theory. Here, we set up a general mathematical model for chemical reaction systems that ...[more]

PMID: 30282809

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Project description:The complement system is part of the innate immune system and plays an important role in the host defense against infectious pathogens. One of the main effects is the opsonization of foreign invaders and subsequent uptake by phagocytosis. Due to the continuous default basal level of active complement molecules, a tight regulation is required to protect the body's own cells (self cells) from opsonization and from complement damage. A major complement regulator is Factor H, which is recruited from the fluid phase and attaches to cell surfaces where it effectively controls complement activation. Besides self cells, pathogens also have the ability to bind Factor H; they can thus escape opsonization and phagocytosis causing severe infections. In order to advance our understanding of the opsonization process at a quantitative level, we developed a mathematical model for the dynamics of the complement system-termed DynaCoSys model-that is based on ordinary differential equations for cell surface-bound molecules and on partial differential equations for concentration profiles of the fluid phase molecules in the environment of cells. This hybrid differential equation approach allows to model the complement cascade focusing on the role of active C3b in the fluid phase and on the cell surface as well as on its inactivation on the cell surface. The DynaCoSys model enables us to quantitatively predict the conditions under which Factor H mediated complement evasion occurs. Furthermore, investigating the quantitative impact of model parameters by a sensitivity analysis, we identify the driving processes of complement activation and regulation in both the self and non-self regime. The two regimes are defined by a critical Factor H concentration on the cell surface and we use the model to investigate the differential impact of complement model parameters on this threshold value. The dynamic modeling on the surface of pathogens are further relevant to understand pathophysiological situations where Factor H mutants and defective Factor H binding to target surfaces results in pathophysiology such as renal and retinal disease. In the future, this DynaCoSys model will be extended to also enable evaluating treatment strategies of complement-related diseases.

Dataset Information

Mathematical modeling reveals spontaneous emergence of self-replication in chemical reaction systems.

Publications

Mathematical modeling reveals spontaneous emergence of self-replication in chemical reaction systems.

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