Abstract
Replicate populations of natural and experimental organisms often show evidence of parallel genetic evolution, but the causes are unclear. The wrinkly spreader morph of Pseudomonas fluorescens arises repeatedly during experimental evolution. The mutational causes reside exclusively within three pathways. By eliminating these, 13 new mutational pathways were discovered with the newly arising WS types having fitnesses similar to those arising from the commonly passaged routes. Our findings show that parallel genetic evolution is strongly biased by constraints and we reveal the genetic bases. From such knowledge, and in instances where new phenotypes arise via gene activation, we suggest a set of principles: evolution proceeds firstly via pathways subject to negative regulation, then via promoter mutations and gene fusions, and finally via activation by intragenic gain-of-function mutations. These principles inform evolutionary forecasting and have relevance to interpreting the diverse array of mutations associated with clinically identical instances of disease in humans.
Highlights
Prediction of evolutionary change from a set of first principles, even in the most elementary of biological systems, has proven difficult
Understanding genetic evolution requires knowledge of the factors that affect the translation of mutation into phenotypic variation
While much is known about the nature of mutation (Drake et al, 1998), knowledge of how change in DNA sequence is translated into phenotypic variation—the raw material for natural selection—is less well understood (Gompel and Prud’homme, 2009)
Summary
Prediction of evolutionary change from a set of first principles, even in the most elementary of biological systems, has proven difficult (de Visser and Krug, 2014). This is due in part to the stochastic nature of mutation, and to lack of understanding of the molecular properties of gene products and their interactions, that is, the processes underpinning development of phenotypes—including genetic and developmental constraints—which are themselves a product of the genotype-to-phenotype map (Pigliucci, 2010). Evolution proceeds along a single pathway and yet that pathway is just one of a number of possible routes to a range of phenotypes with equivalent fitness, determining the underlying causes becomes a matter of interest.
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