PT  - JOURNAL ARTICLE
AU  - BJ Arnold
AU  - MU Gutmann
AU  - YH Grad
AU  - SK Sheppard
AU  - J Corander
AU  - M Lipsitch
AU  - WP Hanage
TI  - Weak epistasis may drive adaptation in recombining bacteria
AID  - 10.1101/119958
DP  - 2017 Jan 01
TA  - bioRxiv
PG  - 119958
4099  - http://biorxiv.org/content/early/2017/03/23/119958.short
4100  - http://biorxiv.org/content/early/2017/03/23/119958.full
AB  - The impact of epistasis on the evolution of multilocus traits depends on recombination. Population genetic theory has been largely developed for eukaryotes, many of which recombine so frequently that epistasis between polymorphisms has not been considered to play a large role in adaptation and has been compared to the fleeting influence of non-heritable effects. Many bacteria also recombine, some to the degree that their populations are described as ‘panmictic’ or ‘freely recombining’. However, whether this recombination is sufficient to limit the ability of selection to act on epistatic contributions to fitness is unknown. We create a sensitive method to quantify homologous recombination in five bacterial pathogens and use these parameter estimates in a multilocus model of bacterial evolution with additive and epistatic effects. We find that even for highly recombining species (e.g. Streptococcus pneumoniae or Helicobacter pylori), selection may act on the cumulative effects of weak (as well as strong) interactions between distant mutations since homologous recombination typically transfers only short segments. Furthermore, whether selection acts more efficiently on physically proximal loci depends on the average recombination tract length. Epistasis may thus play an important role in the adaptive evolution of bacteria and, unlike in eukaryotes, does not need to be strong, involve near loci, or require specific metapopulation dynamics.