Notes and Discussion Points--Biek et al. Paper


    Week 1 and 2


    -study of mutations in bacteria and viruses to find transmission points

    -RNA mutates faster than DNA, so there are more mutations per portion of genomic material than there are in DNA, however, DNA has more genomic material, so there are still just as many mutations just spaced further apart.

    -Fixation is when the frequency of an allele in a population reaches 1. If the allele frequency reaches 0, then it is "lost."

    -Fixation allows us to genealogically find isolates, which act as time and place stamps. These are transfer points that may show how/when a pathogen spread. Fast rates of fixation can allow for smaller time scales, while slow rates of fixation require larger time scales and cannot be used to compare a pathogen moving from, for example, one school to another.

    Antibiotic-use is changing our microbiomes for the worse, and this change helps us learn what effects bacteria has other than making us sick. Even "harmful" bacteria serves multiple functions inside human bodies, such as protecting against other diseases and controlling appetite. An example is the eradication of the Helicobacter pylori, which causes gastritis and peptic ulcers. What people didn't know about H. pylori was that other than causing ulcers, it also regulates ghrelin. Those without H. pylori have much higher levels of ghrelin in their bloodstreams, so those individuals tend to overeat.

    Download file "WEEK 1 - germs_r_us.pdf"

    -Phylogenetic Topology is how a phlyogeny looks, and from the shape we can infer additional information including whether a population is growing, changing, or missing relatives. (A phylogeny is a hypothesis.) Phylogenetic trees can look different depending on what was used to construct it, such as maternal inheritance or bi-parental inheritance.

    Biological complexities

    Intra-genomic and temporal variation in evolutionary rate

    • rate heterogeneity within species
      • variation explained partly by lack of understanding about mutation regulated by DNA repair mechanisms
      • can bacteria differentially control mutation frequency?
    • temporal variation
      • hypermutation - increase substitution rate
      • expect difference between evolutionary rates of bacteria in latent and active replication phases
    • difficult to represent with clock models, can obscure measurable evolutionary signal

    Homologous recombination

    • non-random genomic diversification
      • more frequent exchanges between close relatives
    • rate can vary among and within species, lineages, and genomes
    • can't be ignored, difficult to account for -- improved methods needed
      • sometimes detected if different genome regions support different phylogenetic topologies
        • define phylogenetic topology?
      • can create false mutational signal

    Variation in genome content

    • "core genome" versus "pan-genome"
    • can only study measureably evolving populations using homologous alignments -- apply only to core genome
    • strategies to generate homologous alignments
      • find homologous genes, align them separately
      • align each genome with a reference
    • must do this because one can't ignore gene content variation
      • similar to how natural selection/adaptive forces require genetic variation to proceed?


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