The influence of horizontal gene transfer on the mean fitness of unicellular populations in static environments

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Abstract

Horizontal gene transfer (HGT) is believed to be a major source of genetic variation, particularly for prokaryotes. It is believed that horizontal gene transfer plays a major role in shaping bacterial genomes and is also believed to be responsible for the relatively rapid dissemination and acquisition of new, adaptive traits across bacterial strains. Despite the importance of horizontal gene transfer as a major source of genetic variation, the bulk of research on theoretical evolutionary dynamics and population genetics has focused on point mutations (sometimes coupled with gene duplication events) as the main engine of genomic change. Here, we seek to specifically model HGT processes in bacterial cells, by developing a mathematical model describing the influence that conjugation-mediated HGT has on the mutation-selection balance in an asexually reproducing population of unicellular, prokaryotic organisms. It is assumed that mutation-selection balance is reached in the presence of a fixed background concentration of antibiotic, to which the population must become resistant to survive. We find that HGT has a nontrivial effect on the mean fitness of the population. However, one of the central results that emerge from our analysis is that, at mutation-selection balance, conjugation-mediated HGT has a slightly deleterious effect on the mean fitness of a population. Therefore, we conclude that HGT does not confer a selection advantage in static environments. Rather, its advantage must lie in its ability to promote faster adaptation in dynamic environments, an interpretation that is consistent with the observation that HGT can be promoted by environmental stresses on a population. Copyright © 2010 by the Genetics Society of America.

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Raz, Y., & Tannenbaum, E. (2010). The influence of horizontal gene transfer on the mean fitness of unicellular populations in static environments. Genetics, 185(1), 327–337. https://doi.org/10.1534/genetics.109.113613

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