1. Genotypic Context and Epistasis in Individuals and Populations
Timothy B. Sackton, Daniel L. Hartl 
Cell 
Volume 166, Issue 2, Pages (July 2016)
DOI: /j.cell
Copyright © 2016 Elsevier Inc. Terms and Conditions

2. Figure 1
Hierarchical Fitting of Variance Components Obscures Physiological Epistasis in Population Studies
(A) Genotype-phenotype correspondence in a model of complementary epistasis, in which the phenotypes of genotypes A– B– are assigned values of +1 and genotypes aa– –, – –bb, and aa bb are assigned values −1 (as in Table 1). Genotypes are represented as brown spheres, and the deviation of each phenotypic value from the population mean is shown as a brown dashed line. The frequencies of A and B both set equal to 0.459, as in Crow and Kimura (1970, p. 176). The average of the squared deviations is the total genetic variance, in this case equal to
(B) The plane is the least-squares fit to an additive model of gene action. The black spheres are the predicted phenotypes based on an additive model, and the additive genetic variance is the variance among these predicted phenotypes (in this example 0.582).
(C) The red spheres depict the predicted phenotypes based on a model that includes additive as well as dominance effects but no epistasis. The dashed red lines are the deviations from the additive model due to dominance. The dominance variance equals the average of these squared deviations, in this case After allocating the additive and dominance variance, the remaining variance is the epistatic variance (statistical epistasis), which is a mere 17.1% of the total genetic variance.
Cell  , DOI: ( /j.cell )
Copyright © 2016 Elsevier Inc. Terms and Conditions