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Epistasis is often portrayed as unimportant in evolution. While random patterns of epistasis may have limited effects on the response to selection, systematic directional epistasis can have substantial effects on evolutionary dynamics. Directional epistasis occurs when allele substitutions that change a trait also modify the effects of allele substitution at other loci in a systematic direction. In this case, trait evolution may induce correlated changes in allelic effects and additive genetic variance (evolvability) that modify further evolution. Although theory thus suggests a potentially important role for directional epistasis in evolution, we still lack empirical evidence about its prevalence and magnitude. Using a new framework to estimate systematic patterns of epistasis from line-crosses experiments, we quantify its effects on 197 size-related traits from diverging natural populations in 24 animal and 17 plant species. We show that directional epistasis is common and tends to become stronger with increasing morphological divergence. In animals, most traits displayed negative directionality toward larger size, suggesting that epistatic constraints reducing evolvability toward larger size. Dominance was also common but did not systematically alter the effects of epistasis. [ABSTRACT FROM AUTHOR]

A fundamental aim of post‐genomic 21st century biology is to understand the genotype–phenotype map (GPM) or how specific genetic variation relates to specific phenotypic variation. Quantitative genetics approximates such maps using linear models, and has developed methods to predict the response to selection in a population. The other major field of research concerned with the GPM, developmental evolutionary biology, or evo‐devo, has found the GPM to be highly nonlinear and complex. Here, we quantify how the predictions of quantitative genetics are affected by a complex, nonlinear map based on the development of a multicellular organ. We compared the predicted change in mean phenotype for a single generation using the multivariate breeder's equation, with the change observed from the model of development. We found that there are frequent disagreements between predicted and observed responses to selection due to the nonlinear nature of the genotype–phenotype map. Our results are a step toward integrating the fields studying the GPM. [ABSTRACT FROM AUTHOR]

Phenotypic traits do not always respond to selection independently from each other and often show correlated responses to selection. The structure of a genotype-phenotype map (GP map) determines trait covariation, which involves variation in the degree and strength of the pleiotropic effects of the underlying genes. It is still unclear, and debated, how much of that structure can be deduced from variational properties of quantitative traits that are inferred from their genetic (co) variance matrix ( G-matrix). Here we aim to clarify how the extent of pleiotropy and the correlation among the pleiotropic effects of mutations differentially affect the structure of a G-matrix and our ability to detect genetic constraints from its eigen decomposition. We show that the eigenvectors of a G-matrix can be predictive of evolutionary constraints when they map to underlying pleiotropic modules with correlated mutational effects. Without mutational correlation, evolutionary constraints caused by the fitness costs associated with increased pleiotropy are harder to infer from evolutionary metrics based on a G-matrix's geometric properties because uncorrelated pleiotropic effects do not affect traits' genetic correlations. Correlational selection induces much weaker modular partitioning of traits' genetic correlations in absence then in presence of underlying modular pleiotropy. [ABSTRACT FROM AUTHOR]

Organisms are built from thousands of genes that interact in complex ways. Still, the mathematical theory of evolution is dominated by a gene-by-gene perspective in which genes are assumed to have the same effects regardless of genetic background. Gene interaction, or epistasis, plays a role in some theoretical developments such as the evolution of recombination, reproductive isolation, and canalization, but is strikingly missing from our standard accounts of phenotypic adaptation. This absence is most puzzling within the field of quantitative genetics, which, despite its polygenic perspective and elaborate statistical representation of epistasis, has not found a single important role for gene interaction in evolution. To the contrary, there is a widespread consensus that epistasis is evolutionary inert, and that all we need to know to predict evolutionary dynamics is the additive component of the genetic variance. This view may have roots in convenience, but also in theoretical results showing that the response to selection derived from epistatic variance components is not permanent and will decay when selection is relaxed. I show that these results are tied to a conceptual confusion, and are misleading as general statements about the significance of epistasis for the selection response and adaptation. [ABSTRACT FROM AUTHOR]