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Stop codon reassignments are widely distributed in prokaryotic, eukaryotic and organellar genomes, but are remarkably convergent in terms of the stop codons and amino acids reassigned. Strikingly, the identities of stop codon reassignments are closely matched to the properties of naturally occurring nonsense suppressor (NONS) tRNAs, suggesting that pre-existing nonsense suppression in an ancestral tRNA facilitated the occurrence of stop codon reassignments. Here this idea is expanded, by exploring the mechanism by which the gene duplication of tRNAs has occurred, leading to the reassignment of stop codons. Two types of stop codon reassignment are identified: those that necessitate a tRNA gene duplication, and those that do not because a single tRNA can recognize the reassigned stop codon and the canonical codon(s) for the cognate amino acid. Where tRNA gene duplication has occurred, this implies a multi-functional ancestral NONS tRNA, followed by adaptive mutation in the anticodon of one of the gene duplicates to become complementary to the stop codon, constituting a clear example of escape from adaptive conflict. The best exemplar is the UAA+UAG →gln reassignment, which has occurred 9 times independently in a diverse range of genomes, and appears to reflect the widespread occurrence of naturally occurring nonsense suppression of the UAA+UAG stop codons by glutamine tRNAs. Consideration of pre-existing tRNA functionality and the mechanism of gene duplication provide new insights into the process of stop codon reassignment., (Copyright © 2017 Elsevier B.V. All rights reserved.)

The concept of a 'proteomic constraint' proposes that the information content of the proteome exerts a selective pressure to reduce mutation rates, implying that larger proteomes produce a greater selective pressure to evolve or maintain DNA repair, resulting in a decrease in mutational load. Here, the distribution of 21 recombination repair genes was characterized across 900 bacterial genomes. Consistent with prediction, the presence of 17 genes correlated with proteome size. Intracellular bacteria were marked by a pervasive absence of recombination repair genes, consistent with their small proteome sizes, but also consistent with alternative explanations that reduced effective population size or lack of recombination may decrease selection pressure. However, when only non-intracellular bacteria were examined, the relationship between proteome size and gene presence was maintained. In addition, the more widely distributed (i.e. conserved) a gene, the smaller the average size of the proteomes from which it was absent. Together, these observations are consistent with the operation of a proteomic constraint on DNA repair. Lastly, a correlation between gene absence and genome AT content was shown, indicating a link between absence of DNA repair and elevated genome AT content., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Total evidence and the use of large datasets to overcome uncertainty are the state of the art in systematic analysis. This assumes that the only true phylogenetic signal is ancestry and that functional, structural, and other factors will not add an alternative signal. Using gene families, where individual codon positions were sorted into bins based upon average-pairwise dN/dS ratio, we show that standard, common phylogenetic methods that were designed for stochastic, neutral, site-independent processes, generate less robust phylogenetic signal for bins with strong negative or positive selection. This was true for phylogenetic reconstruction with parsimony, distance, and likelihood methods. Further, we present a case for the potential existence of systematic functional or structural signal that competes with ancestral signal. For the example of positive selection, we simulate the evolution of sequences through three dimensional lattice constructs with folding constraint and changing binding functionality and show that total evidence for these lattice genes presents trees with functional signal, but that the neutral synonymous sites in these genes show the true ancestral signal. In this case, sequence convergence is promoted by functional convergence.