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If the needed secondary mutations are sufficiently common and have a sufficient effect on growth, colony appearance is stimulated by secondary mutations that arise with no required increase in mutation rate.

However, whether these mutations are sufficiently severe to cause the range of aging effects has been questioned [ 24].

However, as much as 33% of nonsynonymous mutations are sufficiently weakly selected to segregate at low frequency in the polymorphism, which is much greater than usually reported.

In fact, these data suggest that at least 49.6% of frameshift mutations are sufficiently deleterious to be removed by natural selection, even under a regime of intense bottlenecking.

We conclude that, despite historical differences in N e for the two species, most newly arising nonsynonymous mutations are sufficiently strongly selected that these differences have played little role in the dynamics of protein evolution.

Similar(55)

Many somatic mutations were sufficiently close to heterozygous germline SNPs that individual sequence read pairs spanned both, thus allowing the mutation to be phased with the SNP.

Evolutionary rescue therefore requires that the frequency of rescue mutations is sufficiently high, Φ > −[ r0/ r0 − r1)][ln (1– P)]/(2 N0 U).

Therefore, the sampling of mutations is sufficiently complete to provide information on the effects of most amino-acid mutations when the data from the three experimental replicates are combined.

However, in our study we observed occasional recoveries of the mean population fitness, which can only be obtained when the rate of back mutations is sufficiently high for offspring to be fitter than the parental generation [ 10].

When a fitness function w (z ) is given and selection and mutation are sufficiently weak, the trait distribution in the offspring pool after mutation, denoted by χ (z ), can be approximated by the following replicator equation plus a mutation term, (4) χ (z ) = ϕ (z ) + [ w (z ) − w − ] ϕ (z ) + μ σ 2 2 ∂ 2 ∂ z 2 ϕ (z ), where w − is the population average of fitness values.

However, within a human cancer, genetic variation due to somatic cell mutation is sufficiently rare that it is impractical to study.

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