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The consistent prediction in mammalian datasets of the G→T,T mutation, ranked second, was unexpected and did not correspond to any characterized mutational bias in mammalian genomes.
We therefore examined if mutational bias in each lineage differed.
Our calculations revealed that there was no CpX or XpC shortage, indicating that the occurrence of 5-methyldeoxycytidine did not create a mutational bias in the DpAV4a genome.
Knight et al. [13] modeled codon and amino acid usage as a function of GC mutational bias in bacteria, prokaryotes and eukaryotes showing that GC content drives codon and amino acid usage and provide a model of usage by compositional class, but did not directly address codon bias.
This creates a mutational bias in the occurrence of deaminations of cytosine and adenine [ 23- 25].
In contrast, there appeared to be little mutational bias in monocots, where other factors increase the frequency codons ending in G|C.
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Mutation can be no less a directional force if a certain class of mutation (G-to-A, small genomic deletions, intron loss, etc). is more frequent than its reverse (A-to-G, small insertions, intron gain, etc).. Thus, all that is needed for mutation-driven recurrent evolution is that multiple lineages are experiencing similar mutational biases in parallel.
Second, we analyzed mutational biases in HCT116 cells complemented with chromosome 3 (HCT116+chr3).
Although these arise (at least in part) from mutational biases in the underlying genomic sequence, modelled mutational rates were invariably higher in mRNA sequences.
Whatever the underlying cause, these strand-specific mutational biases in the mitochondrial genome undoubtedly generate increased mutational load and nonoptimal codon usage.
In this work, we use synonymous sites to analyze regional mutational biases in 20 mammalian, 27 fungal, and 4 insect genomes.
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