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A few mutations are beneficial, and the viruses that inherit those good mutations can swiftly dominate a viral population.
It is only in the hypoxic environment where oxygen is limiting that the mutations are beneficial to cellular proliferation (figure 4).
So, although elevating the mutation rate may reduce fitness through the influx of deleterious mutations, as fitness declines the ratio of beneficial to deleterious mutations may shift to a point at which a significant proportion of new mutations are beneficial, or compensatory, and their collective effects begin to elevate fitness.
Sign epistasis - which occurs when mutations are beneficial in one background and deleterious in other backgrounds - introduces particularly strong constraints.
All mutations are beneficial, and the effects of each mutation (S) are drawn from a continuous distribution f(S).
If covariance is high, then we expect populations to follow very similar trajectories, since the same mutations are beneficial or deleterious in each environment.
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Some mutations were beneficial only if the bacteria already carried other mutations.
While each of the single mutations was beneficial, the fitness effects were not additive.
Surprisingly, most of the detected mutations were beneficial, indicating that selection works more quickly than expected.
Each of these mutations was beneficial alone, but the double mutant was no more fit than the besAE2 single mutant.
Furthermore, we found that at least 0.64% of mutations were beneficial and probably fixed due to positive selection.
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