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The strong dependence on motif and initial length implies that the average genome mutation rate depends on the relative frequency of the various motif types and on the distribution of allele sizes currently segregating in the population.
This, however, is unlikely since the mutation rate depends mainly on the viral reverse transcriptase enzyme, which was identical in all situations.
The rate of a protein's evolution relative to the mutation rate depends on the distribution of fitness effect among mutant sequences.
The optimum mutation rate depends almost exclusively on the effects of beneficial mutations regardless of the extent of deleterious mutation effects.
First, the lower bound on the mutation rate depends not just on the magnitude of Δ U that is accomplishable for antimutator alleles but also on the net rate of mutational production of such alleles.
However, heterozygosity estimates from markers with different mutation rates cannot be compared directly and do not obey a simple scaling rule; how heterozygosity scales with mutation rate depends on the detailed shape of the underlying gene genealogy (and thus on the distribution of time to most recent common ancestor, TMRCA).
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I thought that the mutation rate depended on generations.
Though seed treatment with ultra-violet radiation had not been found effective, pre- or post-treatments with X-rays have been found to decrease or increase X-ray-induced mutation rate (depending on the X-ray dose) in hexaploid wheat4,5 and oats6.
No significant difference in mutation rate depending upon the presence of flanking putative miR binding sites was observed when loci of the same length were compared.
This optimum mutation rate depended on the influx of favorable mutations as well as on their corresponding effects.
The optimum mutation rate depended on both the fraction and the effects of beneficial mutations, rather than on the effects of deleterious ones.
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