Figure 5.—
The distribution of sup and the role of genetic variation. (A) A three-dimensional representation of a sterile trajectory (in this case, involving clonal interference) showing that sup is a measure of the fitness of the sterile lineage relative to the population mean fitness at the time the sterile mutation arose. That is, sup is the sum of the fitness of the background in which the sterile mutation occurred and of the fitness advantage provided by the sterile mutation itself. (B) The distribution of fitness effects of the sterile mutation alone in the ancestral background (sste, gray bars) centers on 0.6% (top) and 1.5% (bottom) in the RM and BY lines, respectively. In all four regimes, however, the initial rate of spread of sterile mutations (sup, orange bars) is faster than can be explained by the effect of the sterile mutation alone, sup > sste (P = 2.5 × 10−7, 2.7 × 10−3, 4.4 × 10−9, and 2.6 × 10−3, for 0.6% small Ne, 1.5% small Ne, 0.6% big Ne, and 1.5% big Ne, respectively, two-tailed t-test, unequal variance). Surprisingly, the distribution of sup is independent of the fitness advantage of the sterile mutation itself (P = 0.66 and P = 0.13 for the hypothesis that sup depends on fitness for big and small Ne, respectively, two-tailed t-test, unequal variance). The eight populations in which steriles swept to fixation are indicated by open blue circles; three of these have sup > 4%. The open circles and horizontal bars indicate the means and standard deviations of the distributions.