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DOI: http://dx.doi.org/10.7554/eLife.07361.003 Following Peck (1994), we first examine the fate of a single advantageous mutant arising in such a population.
Where marked populations are grown before the initiation of an experiment, the possibility exists of a mutant arising in one marker or another before the experiment is begun.
Consequently, any such selfing mutant arising in an obligate outcrossing population would be unable to spread 'automatically' by a 50% transmission advantage of its (selfing) genes over those of the outcrossers (Jarne & Charlesworth, 1993; Holsinger, 2000).
However, in cases where the appropriate competitor with which to compete is unclear or difficult to obtain (for example, a mutant arising in a diverse population or community), growth assays may be the best, albeit not truly accurate, choice.
25 Competitive assays can be a comprehensive and appropriate way to estimate fitness when one is interested in, for example, the fitness of a mutant arising in an isogenic population of wild types.
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In this simulation, the antigenic mutant arises in a genetic background with k = 4 deleterious mutations.
Transient circulation occurs when a small antigenic mutant arises in a good genetic background, provided that it survived genetic drift.
Rapid loss is expected to occur when a small antigenic mutant arises in an average genetic background.
Transient circulation also occurs when a large antigenic mutant arises in an average genetic background, again provided that it survived genetic drift.
We previously demonstrated that a zrt1 Δ etr1 Δ mutant does not bleb [0.09 blebs/colony; Kelly et al. 2011)], indicating that the minisatellite alterations occurring in the zrt1 Δ mutant arise in quiescent cells.
Furthermore, the assay can be used to study the molecular evolution of PR, by replacing the wild-type PR sequence with PR mutants arising in patients, untreated and HAART-treated alike.
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