In contrast, when six oncogenic mutations are required for cancer (C = 6), α50% ranges from 11 30 (Supplementary Table S1), in the lower range of commonly observed values of mutation rate increase due to mutator mutations, suggesting a predominance of mutator pathways, in that most mutator mutations would then correspond to α>α50%.
Most estimates using genetic analysis — looking at the rate of mutations — suggest that they split perhaps 20 million to 30 million years ago, although a few stretch that from 80 million years.
Most are inactivating mutations, suggesting that loss of function may be responsible for the disease phenotype [ 5, 6].
This low yield of simple single mutations suggested that most changes affecting H. pylori Fur's iron-binding pocket were deleterious or lethal, and thus recoverable in transformants only if the fur gene had been inactivated.
A growing body of research on the distribution of fitness effects among beneficial mutations suggests that most have small effects and a few have much larger effects on fitness [ 1, 2].
The effect appeared to be most pronounced in carriers of pathogenic GRN mutations, suggesting a modifying effect of TMEM106B in GRN mutation carriers.
Similar increases in Pen-2 levels were also found with most mutations in TMD2, suggesting a previously unrecognized role of TMD2 in the stability of Pen-2.
Evidence, predominantly from screens of gene knockouts, suggests most mutations affect few traits (Wang et al. 2010; Wagner and Zhang 2011).
Studies in mice suggest that most mutations would be tolerated during developmental processes, but the evolutionary sequence conservation suggests that this is not likely the case.
Our results suggest that most mutations in ACR4 or CR4 TM domains have low to moderate effects on the dimerization potential and that residues in the N-terminal half of the CR4 TM domain are important for dimerization.
