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Updated: Aug 20, 2025

A Micropatterning Assay for Measuring Cell Chirality
Published on: March 11, 2022
Evolutionary Approach to Biological Homochirality
Konstantin K Konstantinov1, Alisa F Konstantinova2
1Softellect Systems, Inc, 414-300 Ave Des Sommets, Verdun, QC, H3E 2B7, Canada. konstantin@softellect.net.
Abstract:
We study a very simple linear evolutionary model based on distribution of protocells by total enantiomeric excess and without any mutual inhibition and show that such model can produce two species with values of total enantiomeric excess in each of the species approaching [Formula: see text] when there is a global [Formula: see text] symmetry. We then consider a scenario when there is a small external global asymmetry factor, like weak interaction, and show that only one of the species remains in such a case, and that is the one, which is more efficient in replication. We perform an estimate of the time necessary to reach homochirality in such a model and show that reasonable assumptions lead to an estimate of around 300 thousand years plus or minus a couple of orders of magnitude. Despite this seemingly large time to reach homochirality, the model is immune to racemization because amino acids in the model follow the lifespan of the protocells rather than the time needed to reach homochirality. We show that not needing mutual inhibition in such evolutionary model is due to the difference in the topology of the spaces in which considered model and many known models of biological homochirality operate. Bifurcation-based models operate in disconnected zero-dimensional space (the space is just two points with enantiomeric excess equal [Formula: see text] and [Formula: see text]), whereas considered evolutionary model (in its continuous representation) operates in one-dimensional connected space, that is the whole interval between [Formula: see text] and [Formula: see text] of total enantiomeric excess. We then proceed with the analysis of the replication process in non-homochiral environment and show that replication errors (the probability to attach an amino acid of wrong chirality) result in a smooth decrease of replication time when total enantiomeric excess of the replicated structure moves away from zero. We show that this decrease in replication time is sufficient for considered model to work.
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