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Accelerated simulation of evolutionary trajectories in origin-fixation models.

ABSTRACT: We present an accelerated algorithm to forward-simulate origin-fixation models. Our algorithm requires, on average, only about two fitness evaluations per fixed mutation, whereas traditional algorithms require, per one fixed mutation, a number of fitness evaluations of the order of the effective population size, Ne Our accelerated algorithm yields the exact same steady state as the original algorithm but produces a different order of fixed mutations. By comparing several relevant evolutionary metrics, such as the distribution of fixed selection coefficients and the probability of reversion, we find that the two algorithms behave equivalently in many respects. However, the accelerated algorithm yields less variance in fixed selection coefficients. Notably, we are able to recover the expected amount of variance by rescaling population size, and we find a linear relationship between the rescaled population size and the population size used by the original algorithm. Considering the widespread usage of origin-fixation simulations across many areas of evolutionary biology, we introduce our accelerated algorithm as a useful tool for increasing the computational complexity of fitness functions without sacrificing much in terms of accuracy of the evolutionary simulation.

SUBMITTER: Teufel AI

PROVIDER: S-EPMC5332577 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature

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Publications

Accelerated simulation of evolutionary trajectories in origin-fixation models.

Teufel Ashley I AI Wilke Claus O CO

Journal of the Royal Society, Interface 20170201 127

We present an accelerated algorithm to forward-simulate origin-fixation models. Our algorithm requires, on average, only about two fitness evaluations per fixed mutation, whereas traditional algorithms require, per one fixed mutation, a number of fitness evaluations of the order of the effective population size, <i>N</i><sub>e</sub> Our accelerated algorithm yields the exact same steady state as the original algorithm but produces a different order of fixed mutations. By comparing several releva ...[more]

PMID: 28228542

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Project description:Understanding how novel functions evolve (genetic adaptation) is a critical goal of evolutionary biology. Among asexual organisms, genetic adaptation involves multiple mutations that frequently interact in a non-linear fashion (epistasis). Non-linear interactions pose a formidable challenge for the computational prediction of mutation effects. Here we use the recent evolution of ?-lactamase under antibiotic selection as a model for genetic adaptation. We build a network of coevolving residues (possible functional interactions), in which nodes are mutant residue positions and links represent two positions found mutated together in the same sequence. Most often these pairs occur in the setting of more complex mutants. Focusing on extended-spectrum resistant sequences, we use network-theoretical tools to identify triple mutant trajectories of likely special significance for adaptation. We extrapolate evolutionary paths (n?=?3) that increase resistance and that are longer than the units used to build the network (n?=?2). These paths consist of a limited number of residue positions and are enriched for known triple mutant combinations that increase cefotaxime resistance. We find that the pairs of residues used to build the network frequently decrease resistance compared to their corresponding singlets. This is a surprising result, given that their coevolution suggests a selective advantage. Thus, ?-lactamase adaptation is highly epistatic. Our method can identify triplets that increase resistance despite the underlying rugged fitness landscape and has the unique ability to make predictions by placing each mutant residue position in its functional context. Our approach requires only sequence information, sufficient genetic diversity, and discrete selective pressures. Thus, it can be used to analyze recent evolutionary events, where coevolution analysis methods that use phylogeny or statistical coupling are not possible. Improving our ability to assess evolutionary trajectories will help predict the evolution of clinically relevant genes and aid in protein design.

Dataset Information

Accelerated simulation of evolutionary trajectories in origin-fixation models.

Publications

Accelerated simulation of evolutionary trajectories in origin-fixation models.

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