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During adaptation, the effect of mutations is different from their effect at equilibrium, probably due, among others, to differences in the fitness of populations and to changes in the genomic context [ 2, 3].
These results suggest that the etiology of ras mutations is different in these three human neoplasms.
Our results suggest that the accumulation and/or segregation of deleterious mutations is different between the two selfing genotypes of E. paniculata.
Taken together, these data show that the effect on DNA binding of MftR mutations is different from that of the equivalent mutations in HucR or PecS.
Our data show that the experimental design needed to most reliably and cost-effectively identify such mutations is different in each case.
Furthermore, for some genes such as Notch, this definition can be cell-type specific, as the spectrum of mutations is different in blood and solid tumors, with different consequences for the protein.
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In the two species, the mutations are different, and the molecular mechanism by which less melanin is produced is different, too.
Yet even though the squamous cell cancers analyzed in the study often had mutations in genes for these enzymes, the genes and the mutations were different in different patients.
The mean number of mutations was different between African-Americans (151.31) and European-Americans (277.63).
The development of genotypic mutations was different in CSF and plasma, suggesting discordant viral evolution.
All mutations were different, indicating a lack of a founder effect in the form of jackpot mutations.
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