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Because a strain carrying an anonymous TS mutation has relatively little value in an era when genome sequencing has largely replaced genetic mapping, we have endeavored to identify mutations underlying several anonymous TS lethal mutations in Neurospora.
Alternatively, selection can act on standing genetic variation (that is, the beneficial mutation has relatively high frequency) leading to soft sweeps or even maintain variability [ 11- 13].
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His work also demonstrated that most mutations had relatively small effects, such as a change in eye color, and that rather than creating a new species in a single step, mutations served to increase variation within the existing population.
All of these mutations have relatively high levels of VKOR activity in the presence of warfarin.
Deleterious mutations have relatively little effect on the evolution of genetic instability unless selection for additional driver mutations is very weak or if deleterious mutations are very common.
In other ancestral reconstruction studies, function-enhancing mutations have relatively minor effects, all less than a 50-fold gain in kcat/KM (Zhang and Rosenberg, 2002; Voordeckers et al., 2012; Risso et al., 2013).
DOI: http://dx.doi.org/10.7554/eLife.04279.006 10.7554/eLiFigure79.007 Figure 3 figure supplement 1. Mutations have relatively small fitness effects during growth on succinate compared to the benefits of threefold or more on DCM.
Although subsequent studies, using sequential short deletion mutants between E13 and T21 of p6gag, as well as a long fragment deletion mutant (S14 I31 of p6gag), suggested that these mutations had relatively tolerable effects on Gag processing and in vitro viral infectivity, the influences of deletion between P30 Y36 of p6gag, as observed in CRF07_BC in Taiwan, were not addressed.
It was suggested that the (+7C>T) mutation has a relatively high frequency in CLL (2.7%).
Although this mutation has a relatively moderate impact on Creb3l2 activity, it causes severe skeletal defects.
While there is experimental evidence of an association between the BMP signalling proteins and oncogenic Ras, the nature of any interaction of BMP cytokine inactivation and k-ras mutation has been relatively unexplored in human tumours.
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