445 thoughts on “Evolution Visualized

  1. This is a very interesting experiment design. Can anyone explain what mutations are occurring (at the molecular level) that grant increased antibiotic resistance?

  2. JoeCoder,

    This is a very interesting experiment design. Can anyone explain what mutations are occurring (at the molecular level) that grant increased antibiotic resistance?

    The Science paper is behind a paywall, but this article has some of the details:

    Giant Petri Dish Displays Evolution in Space and Time

    Using the easy-to-see evolutionary trajectory of the bacteria as a guide, the researchers isolated and sequenced the charge-leading mutants. They found adaptive mutations in the gene for the proofreading enzyme DNA polymerase III, the target genes of the antibiotics, and in unexpected genes such as those coding for a phosphate transporter and a kinase that don’t have a known function in establishing resistance, hinting at alternative pathways that could arise.

  3. Other scientists have shown this before, albeit not quite in such a beautiful and intuitive way. But the MEGA-plate isn’t just a fancy visual aide. It’s also a valuable research tool. Baym and his colleagues can collect microbes from different places on the plate and sequence their DNA. They can then reconstruct the gradual accumulation of mutations that allowed some bacteria to make it all the way from the safe periphery to the deadly centre. They can work out which mutations matter.

    So, I suppose the sequencing hasn’t been done yet.

    But the discussion of compensating mutations is interesting. That implies double mutations. I don’t see any reference to the actual time involved.

    A pity.

  4. Obviously, all of the lineages are searching for…

    Not to diminish its value as original research, this has got to be the greatest contribution ever to education in evolutionary biology.

    The homogeneous environment (stirred, IIRC) in the long-term evolution experiment of Lenski et al. has always bothered me.

  5. petrushka: I don’t see any reference to the actual time involved.

    Commentary says eleven days. Thanks for finding this. Brilliant visualization of evolution in action.

  6. Tom English,

    I wonder if it could be used / reversed to create harmless bacteria that target E Coli*?

    *Isn’t the accumulation of toxins from E Coli waste a big part of the problem?

  7. It may signify some deeper order or it may just be coincidental but the patterns by which new strains split off and bloomed instantly reminded me of this bifurcation diagram I saw in James Gleick’s Chaos….

  8. Woodbine:
    It may signify some deeper order or it may just be coincidental but the patterns by which new strains split off and bloomed instantly reminded me of this bifurcation diagram I saw in James Gleick’s Chaos….

    Bifurcation was my very first thought, about a quarter of the way into the first video. Whether it’s anything more than a superficial similarity, I won’t hazard to guess.

  9. I’ve now read the paper behind this experiment. Assuming I’ve understood it correctly:

    (1.) The mutations to the DNA repair enzyme increased the mutation rate, so these would be loss of function mutations. Among the various lineages, six different mutations were seen at four different sites: “the mutator phenotype emerged at least six times independently… four different alleles of dnaQ were observed.” Multiple pathways are also indicative of loss of function.

    (2.) The mutations in “unexpected genes such as those coding for a phosphate transporter and a kinase” mentioned above by KiethS are described in the paper as having “a probable loss of function (frameshift or nonsense)”

    (3.) The paper mentions other mutations, including 51 non-synonymous mutations in the folA gene that codes dihydrofolate reductase (DHFR), among the various lineages. Figure 3C. I would be interested in knowing the functional consequences of these mutations. I didn’t see any hints in the paper. But this paper says “point mutations of the chromosomal DHFR have been demonstrated to confer intermediate resistance, such as the S. aureus DHFR (saDHFR) residue Phe 98 to Tyr (F98Y) mutation”

    In this experiment, how many mutations count as gain versus modification versus loss of functional coding elements, per Michael Behe’s definition? This seems to be the key in determining what type of argument (and for what side) can be made.

  10. JoeCoder: This seems to be the key in determining what type of argument (and for what side) can be made.

    Science is very different from debate — even more different than computer science is from coding.

  11. I don’t get it. For evolution, all you need is birth and death. So there must be something else going on here. Therefore ID.

  12. Mung:
    I don’t get it. For evolution, all you need is birth and death. So there must be something else going on here. Therefore ID.

    Quick, search for designers at each of the boundaries of increasing antibiotic density. Mung, go frame by frame and look for teh designer(s).

  13. Is anyone really thinking about what this nice video demonstrates or fails to demonstrate? Or is it just pretty, and involves evolution, therefore snark about ID.

    It’s the same antibiotic in all bands (I presume) just at different concentrations.

    So when they say a band has 10x the concentration a wild type can survive, what does that mean? It can’t mean that the concentration is sufficient to kill all the wild type bacteria, else claiming a 100x concentration is just silly, given that it has the same effect as a 10x concentration.

    Nice video. Nice demo of how well-designed bacteria are. Thanks!

  14. Richardthughes: I’m not surprised the author didn’t put their name on that.

    I was surprised about the lack of uproar here about the article that was pulled down recently over at ENV. Napping were we?

  15. Richardthughes: Mung, go frame by frame and look for teh designer(s).

    They looked oddly like bacteria! Much as human designers look oddly human. It’s amazing you can see one but not the other. 🙂

  16. Mung,

    bacteria designed their own changes. Finally we’re getting some ID substance. Talk us through how it worked. I’d like to know about “smart” bacteria that got it right and “dumb” bacteria than got it wrong.

  17. Mung doesn’t even understand what the word ‘concentration’ means:

    So when they say a band has 10x the concentration a wild type can survive, what does that mean? It can’t mean that the concentration is sufficient to kill all the wild type bacteria, else claiming a 100x concentration is just silly, given that it has the same effect as a 10x concentration.

  18. keiths wrong, as usual. You can visibly see an increase in the concentration of the bacterial, as they had to search more and more intently for a new mutation.

  19. Richardthughes: I’d like to know about “smart” bacteria that got it right and “dumb” bacteria than got it wrong.

    How quickly they drop population thinking when it’s convenient.

  20. Mung: I was surprised about the lack of uproar here about the article that was pulled down recently over at ENV. Napping were we?

    Or your basic premise is wrong, inconceivable.

  21. I don’t think it matters much what Behe defines.

    What might be critical to Behe’s argument is how many different pathways exist.

    This is a rather inexpensive experiment that could be done by an ambitious high school.

    I’m going to bet there are many different pathways.

  22. Mung: Nice video. Nice demo of how well-designed bacteria are. Thanks!

    Thanks Designer for such a swell design the better to inflect us. We are special.

  23. newton: We are special.

    I am willing to grant that we would not be here without bacteria. Perhaps that makes them special too.

    By the way, your anthropomorphic definition of antibiotic is noted. But bacteria were here long before we were.

    What was the actual antibiotic used in the research? Was it one used regularly by humans?

  24. Petrushka, I’m talking about Behe’s definition of Functional Coding elemenTs (FCTs), which is entirely separate from his arguments about pathways and simultaneous mutations. See page 420, bottom right, of Behe’s 2010 paper I linked above. If you want a critical perspective, Jerry Coyne reviewed this paper on his blog, including Behe’s definition of FCTs.

    These categories of gain-modification-loss aren’t always cut and dry, as Coyne notes. But if you know a better way to categorize mutations in regard to their functional effects then I’m open to other definitions as well. Behe’s is just the best that I’ve encountered so far.

  25. petrushka: This is a rather inexpensive experiment that could be done by an ambitious high school.

    It is a very dangerous experiment.

    The science is exciting, but the ramifications are horrifying. It’s easy to set up pathways, literally, from single antibiotics to combinations of antibiotics in the agar. I suspect that development of biological weapons just became dirt cheap.

  26. JoeCoder,

    Mutations are helpful or hurtful with respect to the current environment. One need only look at the video. Biochemists will enjoy sorting out the mechanisms, but fitness is just a function of which genomes are reproducing faster in a particular medium.

    Trying to define fitness independent of the environment makes no sense.

  27. JoeCoder: Mung, the experiment used both trimethoprim and ciprofloxacin. But not at the same time I think.

    So they too used an anthropomorphic definition of antibiotic.

    Me, I’d drop the bomb on the little bastards!

  28. Weapons have always been relatively to make, relative to national budgets.

    But it only takes 12 monkeys to type this sonnet.

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