Speaker
Description
Bacterial genes can either reside on the chromosome or on plasmids, extrachromosomal genetic structures that can be transferred from cell to cell. The distribution of genes between plasmid and chromosome is not random: certain types of genes are particularly likely to be plasmid-associated. This includes a number of clinically important traits, such as antibiotic resistance and virulence factors. The evolutionary mechanisms that give rise to this pattern are not well understood. Plasmids are occasionally lost during cell replication and thus less reliably inherited than the chromosome, and genes are free to transition between plasmid and chromosome: so what keeps genes on plasmids? We address this question through mathematical modelling. The key insight from our model is that the relative fitness of chromosomal and plasmid-borne genes depends on their relative frequencies (positive frequency-dependent selection). In other words, the fitness of a plasmid-borne gene will be higher in a population in which the chromosomal gene is rare (and vice versa). This positive frequency dependence can keep moderately beneficial genes on plasmids, despite occasional plasmid loss. This leads to a priority effect: whichever form of the gene (i.e., plasmid-borne or chromosomal) is acquired first has time to increase in frequency and thus becomes difficult to displace. Therefore, the relative rate of acquiring the gene on the plasmid versus the chromosome predicts where the gene will be found. Further modelling shows this effect is particularly pronounced when genes are beneficial across a large number of species. All together, the hypothesis that emerges from our work is that plasmid-borne genes are moderately beneficial; functional across a large number of species; and rarely acquired through chromosomal mutation. We suggest traits like antibiotic resistance are often found on plasmids because these genes commonly fulfil these criteria.
