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This experimental strategy includes a first stage where random mutants are generated and a second phase where mutants are selected under selection pressures imposed by chemical inhibitors of critical steps in the biosynthesis of the target metabolite.

It has been reported that resistant mutants are selected exclusively within a concentration range (mutant selection window) between the mutant prevention concentration (MPC and MICC [ 13, 14].

Drug-resistant mutants are selected by drug pressure in a fraction (termed selection, π, having a value between 50% to 100%) of those individuals who become infected by wild-type virus while on PrEP (e.g. emergence of mutants with: K65R with tenofovir [21] [23]; M184V with emtricitabine [24]; and M184V+K65R with tenofovir+emtricitabine [25], [26]).

Specifically, as viral replication increases, increasing co-infection effectively decreases the pace at which lower fitness mutants are selected against and, therefore, the capacity for high fitness variants to experience selective sweeps.

This has suggested that such mutants are selected for because they impart a relative survival advantage even if they are transformation deficient [10], [14], [15].

These mutants are selected on the basis of their ability to improve cellular phenotypes.

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Similar(51)

Within 400 generations, smaller mutants were selected in response to each size selection.

In that case, 10%% of the mutants were selected per mutation operator.

Mutants were selected by serial transfers in AM1 mineral salts medium with 10% xylose.

Mutants were selected by flow cytometric cell sorting with a fluorescent-labeled SEC3.

Mutants were selected that formed dry, compact, small colonies with reddish-violet pigment on regeneration agar plates.

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