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      Genome-scale rates of evolutionary change in bacteria

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          Abstract

          Estimating the rates at which bacterial genomes evolve is critical to understanding major evolutionary and ecological processes such as disease emergence, long-term host–pathogen associations and short-term transmission patterns. The surge in bacterial genomic data sets provides a new opportunity to estimate these rates and reveal the factors that shape bacterial evolutionary dynamics. For many organisms estimates of evolutionary rate display an inverse association with the time-scale over which the data are sampled. However, this relationship remains unexplored in bacteria due to the difficulty in estimating genome-wide evolutionary rates, which are impacted by the extent of temporal structure in the data and the prevalence of recombination. We collected 36 whole genome sequence data sets from 16 species of bacterial pathogens to systematically estimate and compare their evolutionary rates and assess the extent of temporal structure in the absence of recombination. The majority (28/36) of data sets possessed sufficient clock-like structure to robustly estimate evolutionary rates. However, in some species reliable estimates were not possible even with ‘ancient DNA’ data sampled over many centuries, suggesting that they evolve very slowly or that they display extensive rate variation among lineages. The robustly estimated evolutionary rates spanned several orders of magnitude, from approximately 10 −5 to 10 −8 nucleotide substitutions per site year −1. This variation was negatively associated with sampling time, with this relationship best described by an exponential decay curve. To avoid potential estimation biases, such time-dependency should be considered when inferring evolutionary time-scales in bacteria.

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          Analyzing the mosaic structure of genes.

          Some genes in prokaryotes consist of a mosaic of regions derived from different ancestors by horizontal gene transfer. A method is described for demonstrating the statistical significance of such mosaic structure and for locating the crossover points separating different regions.
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            An exact nonparametric method for inferring mosaic structure in sequence triplets.

            Statistical tests for detecting mosaic structure or recombination among nucleotide sequences usually rely on identifying a pattern or a signal that would be unlikely to appear under clonal reproduction. Dozens of such tests have been described, but many are hampered by long running times, confounding of selection and recombination, and/or inability to isolate the mosaic-producing event. We introduce a test that is exact, nonparametric, rapidly computable, free of the infinite-sites assumption, able to distinguish between recombination and variation in mutation/fixation rates, and able to identify the breakpoints and sequences involved in the mosaic-producing event. Our test considers three sequences at a time: two parent sequences that may have recombined, with one or two breakpoints, to form the third sequence (the child sequence). Excess similarity of the child sequence to a candidate recombinant of the parents is a sign of recombination; we take the maximum value of this excess similarity as our test statistic Delta(m,n,b). We present a method for rapidly calculating the distribution of Delta(m,n,b) and demonstrate that it has comparable power to and a much improved running time over previous methods, especially in detecting recombination in large data sets.
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              Identification of breakpoints in intergenotypic recombinants of HIV type 1 by bootscanning.

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                Author and article information

                Journal
                Microb Genom
                Microb Genom
                MGen
                Microbial Genomics
                Microbiology Society
                2057-5858
                November 2016
                30 November 2016
                : 2
                : 11
                : e000094
                Affiliations
                [ 1]Marie Bashir Institute of Infectious Diseases and Biosecurity, Charles Perkins Centre, School of Life and Environmental Sciences and Sydney Medical School, The University of Sydney , Sydney, NSW 2006, Australia
                [ 2]Centre for Systems Genomics, The University of Melbourne , Melbourne, VIC 3010, Australia
                [ 3]Department of Biochemistry and Molecular Biology, Bio21 Molecular Science and Biotechnology Institute, The University of Melbourne , Melbourne, VIC 3010, Australia
                [ 4]Institut Pasteur, Unité des Bactéries Pathogènes Entériques , Paris 75015, France
                Author notes
                Correspondence Edward C. Holmes ( edward.holmes@ 123456sydney.edu.au )

                All supporting data, code and protocols have been provided within the article or through supplementary

                data files.

                Article
                mgen000094
                10.1099/mgen.0.000094
                5320706
                28348834
                2c698086-8dcb-47af-a5d3-481483303250
                © 2016 The Authors

                This is an open access article under the terms of the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.

                History
                : 16 September 2016
                : 24 October 2016
                Funding
                Funded by: National Health and Medical Research Council
                Award ID: 1061409
                Funded by: National Health and Medical Research Council
                Award ID: GNT1037231
                Categories
                Research Paper
                Microbial Evolution and Epidemiology
                Mechanisms of Evolution
                Custom metadata
                0

                evolution,bacteria,phylogeny,substitution rates,time-dependency,molecular clock

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