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Thus far, efforts to target this mutation over the last two decades have been unsuccessful.
We recalibrate the molecular clock of human mtDNA as 7990 years per synonymous mutation over the mitochondrial genome.
While random mutations and evolutionary drift should not favor one type of mutation over the other one, genes related to pathogenic processes may have evolved recently due to positive selection to fit the pathogenic conditions [ 30].
While cysteamine had no effect on the weight gain of control mice (either WT or heterozygous for the F508del-CFTR mutation) over the experimental period, cysteamine-treated Cftr F508del mice gained significantly (The Student t test, P < 0.01) more weight than did vehicle control Cftr F508del mice (Fig. 2 A and 2B).
Our true wild-type line, in contrast, accumulated only a single mutation over the 170 generations of growth, consistent with previous estimates of the wild-type per-base pair, per-generation mutation rate on the order of 10−10, or one mutation ever few hundred generations (Drake 1991; Lang and Murray 2008; Lynch et al. 2008).
This rate is two orders of magnitude greater than the estimate of 3 × 10−10 mutations per base pair per generation for wild-type yeast strains (Lynch et al. 2008; Nishant et al. 2010); the genomic wild-type strain accumulated only a single mutation over the 170 generations, consistent with a wild-type per-base pair per-generation mutation rate of ~10−10 mutations per base pair per generation.
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If an x or y-value of a prey is on the border of the domain, it can only mutate in one direction (to keep mutation rate constant, mutations over the border will not be neglected, but reflected).
However, experiments involving mtDNA mutator mice have shown a linear progression in the accumulation of mtDNA mutations over the lifespan.
I learned about the character's inception and subsequent, more powerful mutations over the decades.
But flus pick up many mutations over the years, especially when they move back and forth between humans, pigs, birds and other hosts.
Goodman analyzed the distribution of mutations over the span of amino acids in the cytochrome c sequence by distinguishing several different functional groups.
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