445 thoughts on “Evolution Visualized”

  1. Petruska: Here I’m not interested in fitness because its changing effect in regard to the environment makes it a meaningless metric of what evolution can accomplish. Evolution can and sometimes does endlessly destroy genes to increase fitness.

    Rather, what I care about–and what we should all care about–is measuring the rate at which evolution can create specific sequences of information. That’s why I am interested in applying Behe’s definition of FCT’s.

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

    Irrespective of how we got here, ten of eleven cells in your body are bacteria. They are as essential to you as the cells descended from a fertilized human egg. But, of course, any sensible designer would do things that way. Because… Because…

    Help me out, Mung. I’ve read many times that ID provides us with insights into biology that evolutionary theory cannot.

  3. petrushka:
    Weapons have always been relatively to make, relative to national budgets.

    But it only takes 12 monkeys to type this sonnet.

    I was thinking of non-state actors, including one that calls itself a state. I’d forgotten about the movie. (Checking Netflix, I see that I gave it four stars.)

  4. Hi Tom,

    If ID could explain everything, then ID would be a fact, not a theory. So please understand if I cannot explain everything. 🙂

    Irrespective of how we got here, ten of eleven cells in your body are bacteria.

    So if we removed them I would no longer be me. I would, at most, be 1/11th of myself.

    They are as essential to you as the cells descended from a fertilized human egg.

    But the human sperm, and the human egg, and the human zygote, none of those are bacteria? And all the cells that descend from those cells, they are not bacteria?

    Do we become human only when we come to depend on bacteria? There’s a thought to ponder.

    So during the development of the human fetus, at what point do bacteria become the dominant cell type of the body? Never?

    If you ask me, its an absolute miracle that this could happen.

    I’ve read many times that ID provides us with insights into biology that evolutionary theory cannot.

    Evolutionary theory explains this by appealing to “it must have benefited the bacteria” + “it must have benefited the human zygote.”

    I see the theory behind that, what i don’t see is the science behind that.

  5. Mung, no human cells are bacteria because bacteria are prokaryotes (no nucleus) and all animal cells are eukaryotes (have a nucleus). Perhaps you are being facetious, but if so I don’t get your angle?

  6. JoeCoder: Mung, no human cells are bacteria because bacteria are prokaryotes (no nucleus) and all animal cells are eukaryotes (have a nucleus).

    So you agree with Tom that I am only 1/11th me!

    Or perhaps the fact that 10 out of every 11 cells “in my body” are not my body, and that 10 out of every 11 cells “in my body” are not relevant to who I am, and yet it is also the case that “I” would not exist without them,” is a mystery, a miracle.

    But evolutionary theory has an explanation!

    Perhaps you are being facetious

    Both. And.

    We (humans) would not exist if it were not for bacteria. I await for an evolutionary explanation for why not, given that humans originate from a single cell that is not a bacteria.

  9. I say all creos get rid of every bacteria in their bodies. The remaining blob of goo must be their soul. I can see a major oportunity for science advancement here

  10. Mung: So if we removed them I would no longer be me. I would, at most, be 1/11th of myself.

    I count a dead self as no more than zero-elevenths of a self.

    I’ve wondered about the acquisition of gut bacteria by fetuses, but have never bothered to Google. We are born with a kind of shit — I forget the technical term — in our intestines. Breast milk contains nutrients digested by human gut bacteria, and not by human cells. Human gut bacteria are different from the gut bacteria of other mammalian species.

    What looks like coevolution to me no doubt looks like co-design to you.

    ETA: Inter urinas et faeces nascimur.

  13. I’m curious, Mung. Have you finally figured out what the word ‘concentration’ means?

    Or do you still believe the following?

    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.

  14. Mung,

    For evolution, all you need is birth and death.

    Your misrepresentations are getting tiresome. As a minimum you need birth and death.

    [eta – Actually, not strictly necessary. One could instead bring new ones by stork, and send surplus individuals to ‘live on a farm’. Concentration in and removal from the pool is the ting].

  15. Mung,

    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.

    Haha. The ones that didn’t break through weren’t being intent enough.

  16. Mung,

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

    The presence of more than one type is surely indicative of a population property rather than something that ‘only involves individuals’? You and phoodoo are doing brilliantly here.

  21. Mung: 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.

    Not sure who defined antibiotic , sounds more anthropocentric from your objection that bacteria were here in some form first.

  23. Let’s take a moment to say a prayer for the billions of bacteria that died of detrimental mutations trying hard to find something useful. They died in the petri dish so that Mung can call evolution a search. Amen

  25. petrushka: 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.

    I know. I lost a c-note betting on the left side.

    Seriously, very cool video. Thanks for posting it.

    It scared me though.

  26. Big Bang Theory. Hardly an obscure TV show.

    How could anyone interested in science fiction be unaware of the humorous side?

  27. walto: It scared me though.

    I seriously doubt that the dark side is unaware of methods for selecting nasty organisms. But ordinary institutions like hospitals and farms have been running this experiment for decades, perhaps unintentionally.

    Perhaps being able to visualize what is happening will make it easier to oppose bad medical and farming practices.

  29. walto: It scared me though.

    The apparent ease and inevitability of bacteria evolving resistance to antibiotics? The important lesson for us and the use and misuse of antibiotics is to keep antibiotics hidden from bacteria until needed. Antibiotic-resistant bacteria get the opportunity on exposure to sub-lethal doses over time. But there are cost/benefit issues; in an antibiotic-free environment, they are at a disadvantage to wild-type and may go extinct.

  31. Alan Fox: in an antibiotic-free environment, they are at a disadvantage to wild-type and may go extinct.

    Or be reduced to numbers that our immune systems can deal with.

    It would appear that first generation immunity to antibiotics puts the bacterial at a disadvantage, but later mutations can compensate and perhaps evolve into bacteria that have little or no disadvantage.

  32. walto: It scared me though.

    It took a couple hours for the fright to penetrate my fascination. I woke up today thinking about how to obtain antibiotic-resistant strains that remain competitive with wild strains. The truly scary thing is that I’ve come up with several general approaches — literally overnight.

  33. Hence the race to discover antibiotics with novel modes of action.
    Nature is doing your scary work already.

  34. petrushka: Hence the race to discover antibiotics with novel modes of action.

    What race? There’s little economic incentive for the pharmaceutical companies to develop new antibiotics. The UK commissioned a study, not long back, to come up with some means of changing that.

    Here’s a disturbing thought: No one is in a better position to develop antibiotics than the developers of biological weapons. But the military has an incentive to withhold novel antibiotics until they’re desperately needed.

    petrushka: Nature is doing your scary work already.

    The (literal) pathways I’ve designed are unlikely to arise in nature.

  35. I find it odd that with all the governments in the world that provide guaranteed healthcare, none of them sponsor research into antibiotics.

    I see stories that things are being discovered, but it takes money to bring them to the point where they can be used.

  37. petrushka: I find it odd that with all the governments in the world that provide guaranteed healthcare, none of them sponsor research into antibiotics.

    I am not a conspiracy theorist. But I find it implausible that the military forces of economically advanced countries would ignore the threat. They operate as rationally as the big corporations do. The problem is that their objectives align poorly with those shared by most human beings.

    petrushka: I see stories that things are being discovered, but it takes money to bring them to the point where they can be used.

    I also find it implausible that the military would run expensive clinical trials, or rule out use of antibiotics that are not particularly safe. They would think of 100 million deaths in the enemy population versus 10 million deaths in friendly populations as a victory.

  38. JoeCoder:
    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.

    Unless the DNA repair machinery stops working entirely, that’s not necessarily a loss of function. If the ability of the system is reduced so it only detects and repairs (say) 8 out 10, instead of 9 out of 10 mutations, it’s not like the function is lost. Besides, it’s really more of a trade-off if these mutations do indeed contribute to antibiotic resistance.

    Lots of apparently novel phenotypical traits could be described as loss of function in a way that would make it much more apparent that this type of semantical relabeling is just a rhetorical trick to try to emotionally diminish the effect of the evidence for evolution. For example, most semi- and fully aquatic mammals have lost the ability to hunt on land. Where they used to have legs or arms (loss of function), they now have flippers and fins (so actually a trade-off), and many of them have lost their furs (loss of function) for a thick sheath of blubber (so another trade-off).

    In the same way it would be obviously silly to say aquatic mammals, such as whales and dolphins, have suffered “loss of function” mutations for their adaptation to aquatic life, it’s silly here.

    JoeCoder: 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.

    Why?

    JoeCoder: (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)”

    In some way this whole “loss of function” line is rhetorical but vacuous in actual substance. If they all contribute to antibiotic resistance, which in effect means the organism evolves rather than goes extinct, then to call it a loss of function is to miss the point and insist on trying to portray the process through the most negative light possible. For every one of these functions reduced or lost, in so far as they contribute to antibiotic resistance, they enable in increase the function of resistance to the antibiotic.

    JoeCoder: 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.

    I think Behe’s definitions there are mostly fine, with two exceptions.

    First exception is that he defines alterations to an enzyme that allows it to accept a “structurally related substrate” as a “modification-of-function”-mutation.
    That’s ridiculous. If an enzyme’s structure can be altered through mutations such that it can accept another substrate it could not before, then that function is gained regardless of whether the substrate is “structurally related” to the one the enzyme could already access.

    Second exception is that he would consider, for example as mentioned above, the evolution of fins and flippers on aquatic mammals, to be modification rather than gain of function mutations. There’s something specious about a line of argument than would consider the transition from terrestrial to aquatic life merely “modification” rather than “gain”. As I wrote above, I think this is deliberately rhetorical, rather than substantive.

    It seems these labels have more to do with the psychology of IDcreationists than what they do with actual evolutionary biology.

  39. Mung:
    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.

    Yes, I think it demonstates some things and not others. First of all, the main strength of this experiment is that it is so simple and easy to understand. Second, I think it primarily shows the force of random changes subject to environmental selective pressure.

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

    Yes, it goes from initially zero antibiotic in the first section of the gel, to some arbitrary but low concentration in the next, and from there on it is increased tenfold for every new section until the middle.

    So when they say a band has 10x the concentration a wild type can survive, what does that mean?

    I agree that’s badly articulated. I would guess what they meant to say is that it has ten times the concentration of what would be the lethal dosage for wild-type.

    So if the wild-type bacterium is unable to grow at a concentration of 5ug/ml (but CAN grow, but slowly, at 4ug/ml), then 5ug/ml would be the lethal concentration. And if a gel-band has ten times that, it has 50ug/ml.

    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.

    It’s not that simple. At a superficial level yes, if the bacterium can’t grow at 10x concentration, it also can’t grow at 100x concentration. But that doesn’t mean it can grow at 100x concentration just because it can grow at 10x concentration. In fact, that’s what this experiment shows. It has to evolve additional adaptations to be able to grow at a 100-fold concentration, because the antibiotic (apparently) still overwhelms the adaptations gained that allows it to live in a 10-fold lethal-dosage for wild-type. Why that is for this particular experiment I can’t say (haven’t read the papers), you’d have to look into how the actual antibiotic works.

    But I know that some antibiotics work by destabilizing the cell-wall.
    It could be, for example, that the antibiotic destabilizes the cell-wall. So in a low concentration, the wild-type can barely survive. If it were to move into an area with ten times as much antibiotic, it would fully destabilize the wall and kill the bacterium.
    But at the low concentration it can make a living. It lives there for a few generations, the offspring gain some mutations that change the properties of some of the cell-wall-stabilizing proteins, such that it gets more stable again, even with the antibiotic present.
    But if the concentration is now increased again to 100-fold, the mutations are not enough to compensate for the cell-wall being so saturated with antibiotic, so we’re back to the beginning. Additional mutations have to happen before further changes are made to accomodate so much antibiotic infused with the cell-wall. And so on and so forth.

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

    You’d think it wouldn’t have to cost trillions of lives for something well-designed to work properly. No, I think this just shows how the evolutionary process works.

  40. It seems rather typical for IDists to play definition games rather than confront the obvious successes of evolution. Rather rhan marvel at half a dozen consecutive mutations in 11 days, we hear la la la annd the sound of angels being counted on pinheads.

    Whatever happened to isolated islands of function and no stepping stones?

    Any IDists out there care to bet on how many different pathways exist to the center of the medium? Or whether multi-drug resistance can evolve this way?

  41. Rumraket,

    Yes, it goes from initially zero antibiotic in the first section of the gel, to some arbitrary but low concentration in the next…

    It isn’t arbitrary. The concentration in the 1x band is set just high enough to kill the wild-type bacteria. In the words of Baym at around 0:20 in the video, it’s “barely more than the E. coli can survive.”

  42. keiths:
    Rumraket,

    It isn’t arbitrary.The concentration in the 1x band is set just high enough to kill the wild-type bacteria.In the words of Baym at around 0:20 in the video, it’s “barely more than the E. coli can survive.”

    Alright, thank you. I would have guessed they started with something slightly below lethal dosage.

  43. But that doesn’t mean it can grow at 100x concentration just because it can grow at 10x concentration. In fact, that’s what this experiment shows. It has to evolve additional adaptations to be able to grow at a 100-fold concentration

    Do you think the video shows that you cannot get from the wild-type to the 10x strain directly? What would the expected result be if we replaced the 1x band with a 10x band?

  44. Rumraket: I will agree inasmuch that I should’ve distinguished between diminished function and loss of function. I should have said that some of the mutations caused diminished function of DNA repair, not loss. However on the rest I think my definitions make for the most effective benchmark:

    What we are interested in is the rate at which evolution creates useful information. Yes, the “I” word. By information I mean nucleotides that must have a specific sequence in order to perform a function at the molecular level. Like a protein-coding exon, or a binding site. The more specific such a sequence must be, the higher the information density. This is in line with Behe’s definition of FCT’s. If it helps, I disagree with the way most creation and ID proponents ambiguate what does or doesn’t count as information. I’m more generous than that.

    Phenytopic change is only a distraction from this, since information can increase or decrease with almost no detectable effect on phenotype (e.g. gain or loss of a redundant system), or phenotypic fitness can even improve as information is lost, as it often does. At best, the observation of phyenotypic serves as an alert that we should investigate what type of genotypic change is happening.

    Would you at least agree that the benchmark of information is what we should care about? Then we can:

    (1.) Measure how much unique information is in the genomes of various organisms.
    (2.) Use observation and population genetics to estimate the rate at which evolution can create such information. Whether de novo or by modifying existing sequences.
    (3.) Compare the rates of #1 and #2 along with proposed divergence dates to determine if evolution is an adequate explanation of any genomic feature.

    This method will yield false positives for cases where genomic systems cannot be built one mutation at a time, but I think it’s a start.

    “Multiple pathways are also indicative of loss of function–Why?”

    Because there are endless ways to destroy a gene, but very few ways to improve it. If a gene incurs different mutations in different lineages in a short timeframe such as this, it’s probable that the disabling of the gene is being selected for.

  47. Joe coder:

    Good luck trying to quantify information that way.

    It reminds me of counting the characters in a cake recipe.

  48. Mung: Do you think the video shows that you cannot get from the wild-type to the 10x strain directly?

    No it doesn’t show that this isn’t possible. In fact it seems to happen to at least one “lineage” in the experiment as far as I can see, it gets into the 1x band and seems to continue uninhibited into the 10x band.

    However, this is not the case for most of the strains, who seem to halt at each concentration barrier. This is pretty much as expected from an fundamentally stochastic process of mutations having to happen by chance. Once in a while, a lucky individual will recieve the right combination of mutations that allows it to live in high concentrations, without having gone through the selective pressure for a long time. Others are not so lucky, and many generations have to pass before a combination has accumulated that confers increased resistance.

    Mung: Do you think the video shows that you cannot get from the wild-type to the 10x strain directly?

    What would the expected result be if we replaced the 1x band with a 10x band?
    Depends, I think, strongly on the mechanism of action of the antibiotic. A weak rule of thumb that the higher the concentration difference, the more mutations need to happen because more cellular functions are affected. So overall the rate of adaptation would slow down.

  50. Joecoder: What we are interested in is the rate at which evolution creates useful information. Yes, the “I” word. By information I mean nucleotides that must have a specific sequence in order to perform a function at the molecular level. Like a protein-coding exon, or a binding site. The more specific such a sequence must be, the higher the information density.

    Would you at least agree that the benchmark of information is what we should care about?

    If you can give me a way to calculate information content, or information density, we can use right now and apply it to several well-known examples from the literature, I’m all game.

    Unless you have a way of doing such a calculation that isn’t absurdly complicated and doesn’t require a whole lot of ill-defined, vague intuitive judgements, then I don’t see the use of it anyway.

    What I mean is, there’s a genetic sequence, for example the Lac-operon. What’s the information density of the Lac-operon? Calculate it for me and show me your work, then we can talk. Until someone does that, information blather will not impress me and in fact I think it’s completely irrelevant.

    (1.)Measure how much unique information is in the genomes of various organisms.
    (2.)Use observation and population genetics to estimate the rate at which evolution can create such information.Whether de novo or by modifying existing sequences.
    (3.)Compare the rates of #1 and #2 along with proposed divergence dates to determine if evolution is an adequate explanation of any genomic feature.

    I think something like this has already been done to death, using simple informational measures such as bit-size of the genome. Every time this has been done it turns out the nucleotide and genome-size differences are well within plausible evolutionary rates.

    “Multiple pathways are also indicative of loss of function–Why?”

    Because there are endless ways to destroy a gene, but very few ways to improve it.If a gene incurs different mutations in different lineages in a short timeframe such as this, it’s probable that the disabling of the gene is being selected for.

    I understand what you’re saying and I agree. Simply on the basis of empirical studies the most prevalent type of experimental evolution is genome-loss in the sense that deletions are highly favorable in these synthetic, constant environments where the experiments are done.

    It seems to be the rule for bacteria growing in an unchanging flask environment (or in this instance, a nice thick gel) saturated in nutrients, the one main selective pressure that overshadows all others is replication speed.
    The more stuff you can shed under such circumstances, the quicker you can replicate your genome and make a daughter cell. So now there’s two of you to eat the available nutrients before your neighbor does.

    In this experiment, short of the antibiotic itself, there isn’t anything new and there isn’t any changing conditions that would promote much innovation, rather than just increased replication speed. These lab-environments really are highly synthetic compared to, for example, bacteria living in your gut, hundreds of different species coexisting together, where different foods enter every day, in changing quantities and proportions, and you don’t drink the same amount or type of fluids, and don’t eat at exactly the same time and so on and so forth. Or bacteria living in soil, with literally millions of different degrading plant and animal parts surrounding them, daily cycles of temperature, humidity and all of it.

    In so far as a laboratory environment HAS contained something new, a new small molecule as a potential energy source, whether synthetic or natural, or a change in temperature or even the strength of gravity, the bacteria have adapted to it basically every time. Usually with a small degree of innovation (a gene duplication put under a different promoter, or a few mutations that alter an enzyme’s specificity), but combined with a lot of genome-loss for the same reasons as mentioned, even with one single new thing, the synthetic growth environment is constant and unchanging.

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