Abstract
Mutator strains are expected to evolve when the availability and effect of beneficial mutations are high enough to counteract the disadvantage from deleterious mutations that will inevitably accumulate. As the population becomes more adapted to its environment, both availability and effect of beneficial mutations necessarily decrease and mutation rates are predicted to decrease. It has been shown that certain molecular mechanisms can lead to increased mutation rates when the organism finds itself in a stressful environment. While this may be a correlated response to other functions, it could also be an adaptive mechanism, raising mutation rates only when it is most advantageous. Here, we use a mathematical model to investigate the plausibility of the adaptive hypothesis. We show that such a mechanism can be mantained if the population is subjected to diverse stresses. By simulating various antibiotic treatment schemes, we find that combination treatments can reduce the effectiveness of second-order selection on stress-induced mutagenesis. We discuss the implications of our results to strategies of antibiotic therapy.
Highlights
New mutations are the ultimate source of the variation that fuels adaptation
Many organisms display increased mutation or recombination rates when exposed to a stressful environment, which can increase the probability that the population acquires adaptations that allow it to avoid extinction
We provide an explicit expression for the critical time interval between exposures and discuss its implication for the evolution of resistance
Summary
We aim to calculate the SIM allele frequencies pM = pMr + pMR before the onset of each stress period, i.e., at the end of each cycle of stress followed by no stress
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