On the evolution of epistasis III: The haploid case with mutation

Abstract

Whether interaction between genes is better represented by synergistic or antagonistic epistasis has been a focus of experimental research in bacterial population genetics. Our previous research on evolution of modifiers of epistasis in diploid systems has indicated that the strength of positive or negative epistasis should increase provided linkage disequilibrium is maintained. Here we study a modifier of epistasis in fitness between two loci in a haploid system. Epistasis is modified in the neighborhood of a mutation selection balance. We show that when linkage in the three-locus system is tight, an increase in the frequency of a modifier allele that induces either more negative or more positive epistasis is possible. Epistasis here can be measured on either an additive or multiplicative scale.

The Evolution of Epistasis and Its Links With Genetic Robustness, Complexity and Drift in a Phenotypic Model of Adaptation

“…Epistasis is then chosen to be homogenous among loci, being either positive or negative. With this framework it was shown that epistasis could largely influence the way populations would respond to selection (Kimura and Maruyama 1966;Charlesworth 1990;Kauffman 1993;Hansen and Wagner 2001;de Visser and Elena 2007), and some recent studies have shown how natural selection shapes epistasis (Liberman and Feldman 2005, 2006, 2008Desai et al 2007;Liberman et al 2007). However, all experimental data, to date, have found that both kinds of epistasis were present simultaneously (Elena and Lenski 1997;Sanjuan et al 2005;Jasnos and Korona 2007), and therefore such theories should be revisited to see how robust they are to the presence of both kinds of epistasis (Kouyos et al 2006(Kouyos et al , 2007.…”

“…Evolution of the parameter Q depends on drift: Previous studies have analyzed the evolution of epistasis (Liberman and Feldman 2005, 2006, 2008Desai et al 2007;Liberman et al 2007). However, they focused on modifiers of epistasis acting on two loci or on modifiers of epistasis acting on many loci having mutations of similar effects on fitness.…”

“…In previous studies (Liberman and Feldman 2005, 2006, 2008Desai et al 2007;Liberman et al 2007), the theoretical framework used was that of a very large population size and fixed effect of mutations. In such a context, the population remains at the fitness optimum.…”

“…In several systems, such as RNA folding or artificial life (Wilke and Adami 2001), it was found that epistasis was correlated with the mean effect of mutations. On the basis of these observations, analytical models have been developed in which a locus affects the epistatic interactions between mutations at other loci (Liberman and Feldman 2005, 2006, 2008Desai et al 2007;Liberman et al 2007). Our present work extends these theoretical works on modifiers of epistasis to the case of a continuum of mutations effects.…”

Adaptive Partitioning of the tRNA Interaction Interface by Aminoacyl-tRNA-Synthetases

“…Once enough genes came to depend on this code, and cellular fitness increasingly depended on interdependent coordination of the action of many gene products, an evolutionary phase transition occurred that “froze” the genetic code [12, 13]. In parallel, increasingly complex fitness interactions among genes, called generally epistasis [14, 15], cooled the rate of gene sharing, changing the evolution of cells from a genetically communal to a more vertical mode of inheritance in a Statistical Tree of Life [16], in what Woese called the Darwinian Transition . Broadly consistent with this theory, it was found that complexity of gene interactions (the number of pairwise interactions a gene undertakes) constrains “informational” genes from transferring horizontally between cells relative to condition-dependent “operational” genes [17, 18] and increasing pairwise protein-protein interactions, as measured in yeast two-hybrid data, reduces substitution rates in proteins [19].…”