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. 2021 Jan 19;10:e63910. doi: 10.7554/eLife.63910

Figure 7. ADE pathway evolution.

(A) Simplified schematic of the adenine biosynthesis pathway. Circles represent metabolic intermediates; AIR is the toxic metabolic intermediate phosphoribosylaminoimidazole. Annotations represent the number of fixed nonsynonymous mutations in each gene (note that ADE5 and ADE7 are both products of the same gene). (B) Schematic of a fitness landscape with four possible states defined by whether ADE2 is functional and whether the ADE pathway upstream of ADE2 is functional. The small insets represent the state of the pathway in (A) at each position. Elevation in the landscape represents putative fitness differences, and the width of the arrows represents the putative mutation rates between the different states.

Figure 7.

Figure 7—figure supplement 1. Overdispersion.

Figure 7—figure supplement 1.

(A) For each environment-strain combination, we plot the number of genes having a certain number of fixed nonsynonymous mutations (y axis) spread amongst a certain number of unique populations (x axis). Each possible outcome is colored by its excess probability, as compared to a simulated null expectation in which mutations are distributed among populations using a multinomial distribution that takes into account how many nonsynonymous mutations fix in each population. Each plot is annotated with Δm, the difference between the total number of ‘missed opportunities’ as defined by Good et al., 2017 and the average total number of missed opportunities from simulated datasets, along with the probability of finding less than or equal to our total missed opportunities in one of the simulated datasets. The negative values for Δm indicate that we are seeing less missed opportunities than we would expect by chance, indicating overdispersion most likely caused by a ‘coupon collecting’ effect. (B) The same as A, but also including nonsynonymous mutations that are detected but do not fix.
Figure 7—figure supplement 2. Mutual information analysis.

Figure 7—figure supplement 2.

Comparison of the sum of mutual information between all multi-hit genes in our dataset and the mutual information between this set of genes in simulated data based on probabilities assigned to each mutation in each population, allowing for different probabilities in each environment strain combination (see Materials and methods).