Clonal interference in large populations

Clonal interference, the competition between lineages arising from different beneficial mutations in an asexually reproducing population, is an important factor determining the tempo and mode of microbial adaptation. The standard theory of this phenomenon neglects the occurrence of multiple mutation...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 2007-11, Vol.104 (46), p.18135-18140
Main Authors: Park, Su-Chan, Krug, Joachim
Format: Article
Language:English
Subjects:
Adaptation, Physiological - genetics
Animal behavior
Animal populations
Biological Sciences
Coefficients
Correlation analysis
Dispersal
Ecological competition
Evolution
Evolutionary genetics
Genetic drift
Genetic mutation
Genotypes
Microbiology
Models, Theoretical
Mutation
Population distributions
Population mean
Population size
Simulation
Studies
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Summary:Clonal interference, the competition between lineages arising from different beneficial mutations in an asexually reproducing population, is an important factor determining the tempo and mode of microbial adaptation. The standard theory of this phenomenon neglects the occurrence of multiple mutations as well as the correlation between loss by genetic drift and clonal competition, which is questionable in large populations. Working within the Wright-Fisher model with multiplicative fitness (no epistasis), we determine the rate of adaptation asymptotically for very large population sizes and show that the standard theory fails in this regime. Our study also explains the success of the standard theory in predicting the rate of adaptation for moderately large populations. Furthermore, we show that the nature of the substitution process changes qualitatively when multiple mutations are allowed for, because several mutations can be fixed in a single fixation event. As a consequence, the index of dispersion for counts of the fixation process displays a minimum as a function of population size, whereas the origination process of fixed mutations becomes completely regular for very large populations. We find that the number of mutations fixed in a single event is geometrically distributed as in the neutral case. These conclusions are based on extensive simulations combined with analytic results for the limit of infinite population size.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.0705778104