Abstract
Identification of the selective forces contributing to the origin and maintenance of sex is a fundamental problem in biology. The Fisher–Muller model proposes that sex is advantageous because it allows beneficial mutations that arise in different lineages to recombine, thereby reducing clonal interference and speeding adaptation. I used the F plasmid to mediate recombination in the bacterium Escherichia coli and measured its effect on adaptation at high and low mutation rates. Recombination increased the rate of adaptation ∼3-fold more in the high mutation rate treatment, where beneficial mutations had to compete for fixation. Sequencing of candidate loci revealed the presence of a beneficial mutation in six high mutation rate lines. In the absence of recombination, this mutation took longer to fix and, over the course of its substitution, conferred a reduced competitive advantage, indicating interference between competing beneficial mutations. Together, these results provide experimental support for the Fisher–Muller model and demonstrate that plasmid-mediated gene transfer can accelerate bacterial adaptation.
Highlights
Understanding the factors that contribute to the origin and maintenance of sex is an important unanswered problem in evolutionary biology [1,2,3,4]
Why have sex? One explanation is that sex is good because it allows beneficial mutations from different lineages to recombine
Using a simple microbial system I showed that recombination increased the rate of fitness improvement when beneficial mutations were common in the population and had to compete for fixation, but had little effect when mutations occurred rarely
Summary
Understanding the factors that contribute to the origin and maintenance of sex is an important unanswered problem in evolutionary biology [1,2,3,4]. Even in the presence of strong competition between mutations, recombination may not provide a substantial advantage if interactions between mutations cause the advantage conferred by a given mutation to depend on a particular genetic background [31] This might be the case if beneficial mutations tend to occur as part of co-adapted gene complexes. An ideal experimental test of the FM model would compare the effect of recombination on the rate of adaptation in treatments that differ solely in the extent of competition between beneficial mutations. In practice this ideal has been hard to achieve.
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