Lenski experiment and falsifiability

Faith & Science Conversation
41

This example comes up enough that it’s worth commenting on.

This is the prestin gene - a gene that all mammals have and use for hearing. So it’s not like bats and whales came up with it independently.

This gene appears to have undergone convergent evolution at the amino acid level in echolocating bats and whales. Note well - the convergence is at the amino acid level, not at the DNA sequence level.

If you exclude the few amino acids that show convergence and run the phylogenetic tools without those few, the rest of the gene produces the same phylogenetic tree that other sequences do - placing whales and bats as very distant relatives, with whales more closely clustering with other extant artiodactyls.

All of this is what you would predict from convergence, so the hypothesis that what we’re looking at is convergence is very strongly supported.

It’s the “same molecular route” in so far as the two lineages converged on a few amino acid substitutions in a protein they shared and used for hearing.

Any questions?

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You’re assuming that none of these mutations existed prior to the selection for echolocation being applied. Why make that assumption? The lineages leading to both bats and whales would have had diversity within them all along the way.

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43

Would moving through water be a factor?

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Sir, I believe you are referring to the original 2010 study that focused on the single Prestin protein…

https://www.sciencemag.org/news/2010/01/hear-bats-and-whales-share-sonar-protein

“a new study shows that in both groups the same protein evolved in the same way to make that possible. Researchers say it’s surprising to discover a molecular convergence in these very distantly related groups of animals. The protein, called prestin, exists in all mammals…”

https://www.sciencemag.org/news/2013/09/bats-and-dolphins-evolved-echolocation-same-way

“in 2010, Stephen Rossiter, an evolutionary biologist at Queen Mary, University of London, and his colleagues determined that both types of echolocating bats, as well as dolphins, had the same mutations in a particular protein called prestin, which affects the sensitivity of hearing.

But I’m referring to the more recent 2013 study wherein:

Now, Rossiter’s team has expanded the search for this so-called molecular convergence to the entire genome. They sequenced the genomes of four species from various branches of the bat family tree, two that use echolocation and two that don’t. They added in the existing genome sequences of the large flying fox and the little brown bat, another echolocator. Evolutionary biologist Joe Parker, also at Queen Mary, University of London, compared the bat genetic sequences to those from more than a dozen other mammals, including the bottlenose dolphin. He focused on the 2300 genes that exist in single copies in all the bats, the dolphin, and at least five other mammals. He evaluated how similar each gene was to its counterparts in various bats and the dolphin. The analysis revealed that 200 genes had independently changed in the same ways, Parker, Rossiter and their colleagues report today in Nature . Several of the genes are involved in hearing, but the others have no clear link to echolocation so far; some genes with shared changes are important for vision, but most have functions that are unknown.

Thus, I’m basing my understanding on numerous reports of the experiment and what the scientists involved report. For instance…

“We had expected to find identical changes in maybe a dozen or so genes but to see nearly 200 is incredible," explains Dr. Joe Parker, first author on the paper. “We know natural selection is a potent driver of gene sequence evolution, but identifying so many examples where it produces nearly identical results in the genetic sequences of totally unrelated animals is astonishing.”

Dr. Georgia Tsagkogeorga, who undertook the assembly of the new genome data for this study, added, “We found that molecular signals of convergence were widespread, and were seen in many genes across the genome. It greatly adds to our understanding of genome evolution.”

Group leader, Dr. Stephen Rossiter, said, "These results could be the tip of the iceberg. As the genomes of more species are sequenced and studied, we may well see other striking cases of convergent adaptations being driven by identical genetic changes."

  1. Unless my reading comprehension is very suspect, they report identical results “in the gene sequences”, not simply the amino acids. “Identical genetic changes”, “seen in many genes”… etc., etc.

  2. they discovered identical changes in “nearly 200 genes,” and “in many genes across the genome.” not simply the single Prestin gene. For instance:

https://www.sciencemag.org/news/2013/09/bats-and-dolphins-evolved-echolocation-same-way

[The analysis revealed that 200 genes had independently changed in the same ways,](http://dx.doi.org/10.1038/nature12511) Parker, Rossiter and their colleagues report today in Nature . Several of the genes are involved in hearing, but the others have no clear link to echolocation so far; some genes with shared changes are important for vision, but most have functions that are unknown. “The biggest surprise,” says Frédéric Delsuc, a molecular phylogeneticist at Montpellier University in France, “is probably the extent to which convergent molecular evolution seems to be widespread in the genome."

So unless I am not reading something properly, they are referring not simply to amino acid sequence in the prestin hearing gene, but in the genetic sequence of approx 200 genes.

So unless you can further clarify, I stand by my original understanding of what these articles report. That there are ~ 200 genes that “independently changed in the same ways.”

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45

Hi Daniel,

I was talking about both the original prestin work and the later work, because they are related:

The newer paper is also about convergence at the amino acid level. They took the results of the original prestin work and looked to see if other amino acid convergences could be found. Convergences at the amino acid level will usually not have identical DNA underlying them - and that is what we see. The rest of the genes in question, aside from the few convergent amino acids, follow the regular phylogenetic pattern predicted by other characters (other genes, anatomy, etc).

My comment about you expecting de novo mutations also applies to both the original and newer work. You seem to be calculating things based on waiting for each mutation to arise after selection is applied (why?) and you also - unless I’m not reading you correctly because I’m pre-caffeinated at the moment - seem to be basing your calculations on having only one individual in each generation in each lineage (why??). Neither assumption is realistic.

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46

Sir, thank you for your additional insight. You’ll have to explain to me, specifically, why the authors of the study repeatedly refer to “nearly identical results in the genetic sequences” and “driven by identical genetic changes.”

Were they just being that sloppy?

Additionally, can we agree that their study found convergence in ~200 genes, and not in Prestin alone? Thus even if we are talking amino acids, they had to converge in not a few, but bare minimum 200 (though likely far more) amino acid substitutions, no? Or do I misunderstand that aspect as well?

…

As for my math, I gathered from a few sources, but the baseline for populations I use for my personal study is

https://www.pnas.org/content/99/2/803

Our results suggest that the average mammalian genome mutation rate is 2.2 × 10−9 per base pair per year, which provides further opportunities for estimating species and population divergence times by using molecular clocks.

Unless I misunderstand, this regards the population, not simply as regards a single individual organism. And these mutations, by definition, have to arise randomly before natural selection is applied… else natural selection has nothing to select, no? There’s still only a 1 / 450,000,000 chance during any year of any particular required mutation arising (and then the smaller chance of it being the right mutation).

And the timeframe we’re looking at is a mere 5,000,000 years, to see the correct mutation to arise in not merely one, but all 200 genes?

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Hi Daniel,

Thanks for asking questions and good on you for trying to get this sorted out. I will get back to you later, but I have a busy workday ahead of me…

Perhaps @glipsnort or @sfmatheson might have time and inclination to contribute.

As for the “identical genetic sequences” - yes, they’re talking about identical amino acids. Those are a “sequence” and they’re not parsing it down to the DNA level for a popular article.

Mutation rate estimates are not at a population level, no.

Bats and whales have a most recent common ancestor at 5 MYA? What?

More anon.

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48

Brief responses:

  1. The study finding convergent evolution in 200 genes was indeed looking at amino acid sequence, not DNA: “In this method, we examined each amino acid along the alignment of a given CDS…”
  2. Their conclusions have been severely undercut by a subsequent study contradicting theirs: No Genome-Wide Protein Sequence Convergence for Echolocation
  3. There is good evidence for convergent evolution in echo-locating species in 7 genes. (I forget where I gleaned that from – probably the paper I just linked to.)
  4. Yes, the quoted mutation rate is per individual, not per population.
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Interesting, and thanks for the links. I picked that mutation rate as it seemed to be derived from comparing different species and being able to be used for estimate of evolutionary distance.

What would be a good estimate of population wide mutation rates per base pair across the evolutionary timescales?

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if you might be so kind and so inclinded, I wonder if you would look over a yet more recent article on the topic, and see if anything of relevance stands out to you per the discussion?

http://advances.sciencemag.org/content/4/9/eaat9660?rss=1

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Thanks for pointing out that additional study. I was really worried about false positives when looking briefly at the “200 genes paper” but hadn’t had time to dig in.

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If you’re interested in the absolute number of de novo mutations within the population as a whole, ideally you’d use census size. We don’t normally have census size for populations in the past (that’s an understatement, btw) so we might try for effective population size instead, though that will (usually) be an underestimate.

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5MY between whales/dolphins with echolocation and their common ancestor with nonecholocating whales.

Any common/convergent mutations (whether genetic or amino acid level) between bats and echolocating whales, which were not present in nonecholocating whale ancestors, had to arise within that 5MY period.

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For moderate-sized populations, it would just be the per-individual mutation rate times the size of the populations. For very large populations you have to correct for the fact that some mutations will be occurring multiple times in the population.

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I’ll try to look at it, but no guarantees.

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Christy, I’d meant to reply to you earlier…

No, certainly the existence of bacteria over 3.5 billion years wouldn’t falsify evolutionary mechanism. Rather, it would be lack of any significant, novel changes or mutations over that period. Though to my knowledge we have no way of knowing that kind of data over that period… correct me if I’m wrong, but we don’t have any way of determining the precise structure, organelles, proteins, specific genetic changes, etc., from fossilized bacteria.

I’m only curious about what we could in fact observe. - So the only thing we could examine empirically is the bacteria we’ve been able to directly observe.

In other words, I understand there are significant de novo changes, or very, very rapid acccumulation of small coordinated changes all seemingly coordinated, that are required to get from land animals to whales, flightless to flying animals, precise fine tuned echolocation, or even from primitive primates to humans.

If these beneficial, functional, de novo changes are expected to happen in a vastly smaller population over a “mere” 1 million generations or so, I would expect to see some comparable de novo changes during the general timeframe we have been able to empirically observe bacteria and protozoa.

Basically, my impression is that, over all the period over the last ~ 70 years or so we have been able to examine bacteria and protozoa in serial… with huge population sizes and very fast generation times, we have still seen nothing but small changes, the kind that would be insufficient to explain the genetic leaps involved in multicellular animals over comparable generation times.

But some here have said I’m comparing apples and oranges, as bacteria don’t evolve as quickly as multicellular life does, with its smaller genetic code.

My inveterate skepticisms cries “how convenient,” and it seems too much like the superhero from “Mystery Men” who could turn invisible, so long as no one was watching.

multicellular life evolves great novelties in a relatively short amount of generations. But generation times are simply too long to see evolution happen, I am told. OK, I say, let’s see if it happens in an organism we can observe many generations quickly! Oh, no, you can’t see that either, because if they generate fast enough for you to see evolution happen, those organisms evolve too slowly for you to see it.

How convenient for the theory. So evolution happens so long as I’m not watching, it seems. Though I try to maintain an open mind…

But I’d like to have some objective sense, hence my bottom line question…

Over just how many generations, of how many different populations, and what kind of organisms, specifically, would we have to observe organisms remaining essentially unchanged before we could start to legitimately doubt the ability of the “natural selection+variation” mechanism to account for novel complexity in life? Even if we’re talking to collaborated efforts of scientists over the next million years. How long would we have to have observed organisms reproduce but not evolve new complex features?

That is, how many times would we have to ”repeat” and “test” the theory, and observe it fail to produce similar or at least analogous results, for us to consider falsifying the theory?

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First of all … LOVED that movie. I still have visions of Mr. Furious (whose super-hero power is his fantastically volatile temper) jumping up and down with ineffectual rage on the top of the car.

Regarding bacterial evolution … let me try to answer this in more general terms, leaving biological details to those much more knowledgeable in those areas.

I think it is fair to say that evolution is probably “more rapid” (whatever that means) among microbial life than much larger multicellular organisms simply because of the much more rapid reproduction. But it is probably also true that evolution generally fills all the possible niches or “possible domain space” as time goes on (like gas molecules always expanding to fill any container). So just because we still have bacteria today doesn’t mean that there hasn’t been all the requisite evolution from such life at various points in the past. Such microbial life still has a huge niche in today’s world and so that particular niche will continue to be filled with ever more evolved bacteria (that are still bacteria) - just as, after releasing some gas in one part of a container; when we find that gas present on the other side of the container, we wouldn’t then insist that it can no longer be present where it was released. It is all over because any niche that can be filled will then remain filled.

Regarding the “we can’t ever see it when we look”, this may be a bit like taking momentary glances at the hour hand of a clock. People tell you it’s moving. But it never is whenever you look at it. So the only way is to note that “over time” it isn’t where it was before, so it’s disingenuous of me to insist that it isn’t moving if I can’t see it move. That “over time” is no mere human life span in the case of evolution. So our only way to know of movement is to looks at snapshots of the past via the fossil record and many other similar clues.

[…and on the other side of this then - if we do observe actual evolutionary adaptations/changes, even those that might span a few centuries of observation, - then on geological timescales that would qualify as a vastly rapid change to the point of being a cusp on a graph. Just as if you actually do see the hour hand move in a tiny lurch, you were probably lucky to catch it in the act. Such saltational action is part of the whole picture too, if I’ve understood Gould’s contributions rightly.]

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I understand your frustration, but yeah, I think you have unrealistic expectations of the kind of “empirical evidence” you are entitled to in order to feel less skeptical. And I think it is kind of silly to discount observations of the fossil record as observations.

Personally, I keep coming back to the idea that a global conspiracy of biologists for 150 years to dupe the world and maintain a worthless theory simply because they don’t believe in God or design or whatever sounds ridiculous to me. The evolutionary model is well-supported and has not been falsified. Unless scientists come up with something with more explanatory power, it’s the rational option.

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Very much appreciated, and I think I follow you. Let me clarify, and see if I follow you properly, I fear I may not have explained myself properly:

—I have no issue whatsoever with the continued existence of bacteria, or the fact that some bacteria have remained unchanged. If they are “fit” and functional, they will remain. One branch may develop some new and novel feature, but unless its fitness is so significantly greater, or the environment changes to make the previous version significantly less fit, then the old version will certainly stay around.

For instance, in the presence of an antibiotic, ALL the previous versions will die out, and only those with the resistance will remain to continue to live and pass on their genes. But there are certainly cases where a new, novel feature develops, and provides enough of a novel benefit so that the new version will grow and thrive… but there’s nothing in the environment that makes the old version particularly unhealthy, so the previous version will continue to thrive.

I have no issue with that aspect of evolutionary theory at all. When I say I have problem if bacteria remain unchanged for 2 billion years, I mean to say that my problem is if EVERY AND ALL bacteria remained so unchanged for 2 billion years, and NONE of them exhibited ANY change. Surely, some of them are fit enough, have their “niche,” and will continue. But if I observed a population that never evolved a new characteristic whatsoever, this I feel would disprove the basic theory.

That is of course why I fully embrace the basic microevolutionary theory - it is clearly demonstrable, repeatable, testable, and observable. I’ve done it myself. We see it in animal breeding as well as on Petri dishes.

So to summarize by example, and see if you follow my objection: At one point, a bacteria without a flagella evolved to have a flagella. Perhaps the flagella provided such a benefit that all its descendents had an advantage in survival, and thus the population of flagella-bearing bacterial grew and thrived. But this did not mean the previous version was in any way “unfit,” so the previous version, without the flagella, continued unchanged. — This basic concept I have no issue with whatsoever.

My objection would be if we observed a particular population of bacteria for a zillion years, watching zillions times millions of generations and having allowed for billions of zillions of organisms to live and thrive and experience zillions of mutatations, but during that whole period, they never evolved anything novel and complex that was even remotely comparable to a flagella…

At THIS point, I start to doubt whether the proposed mechanism (unguided natural selection acting on random variation) could actually accomplish what it claims to be able to do. It isn’t the continued existence of the old model, it is the failure to produce any new models, from which my skepticism would stem… which leads me to your other points, but I’ll get to those in a separate entry…

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These are very thoughtful and apposite analogies, so if I may respond…

I wouldn’t disagree with this in principle. The difference for me being, with a clock, I can open it up, inspect it, see this gear connected to this one, see that if I move this it moves this one, and there is nothing at all to me that is categorically different that would have to happen that isn’t already built into the mechanism of the clock.

For this reason, I have no issue when people line up multiple fossils of horses, or of elephants and mammoths, or similar dinosaurs, or the like. The micro evolution that creates this very kind of variation is well documented, tested, repeated, utilized, and easily explains that kind of variation, and if there are “gaps” in the fossil record between two such exitinct animals, the process we are capable of observing is an adequate explanation for such, and thus I can assume they are related even if I don’t have a specific fossil.

But then there changes that don’t have that kind of explanation. If someone told me that a digital clock also changes with slow movements… that the digital 2 for instance becomes a 3 by that vertical line on the bottom slowly moving from the left to the right… and I open up the clock and find no mechanism that would account for that movement, then I remain skeptical.

These are the kinds of leaps I see in prokaryotes to Eukaryotes, to multi-celled animals, land animals to whales, echolocation, flight, etc. I do not see a mechanism observed, repeated, tested, etc., that is capable of producing that kind of change.

Which leads to…

We do see some significant changes, certainly. But consider, I could take some work of fiction, create a random letter generator in my computer, and set it up so it cross references the dictionary, and accepts only those variations and mutations and pass that make a new word. Occasionally that may make some impressive changes that are “beneficial” on the micro-level, changing “Brother” to “Bother” or “son” to “sin”. That process could conceivably “improve” Hamlet or Henry V. There are plenty of internet examples where a “mistake” of one letter made what some would call an “improvement” (usually with very comical results). So any particular instance or case is hardly worth disputing.

But if someone tried to tell me that a particular novel had been constructed by using this process, with all the detailed plots, the complex relationships between the characters, the carefully crafted mystery or the flow of the story… I’d remain very skeptical indeed.

That is the basic point at which I lose faith in evolution… when someone points to a small change as “proof” of a large scale macro change; the large change simply explained as being the cumulative effect of the small changes we are able to witness, no?

By that logic, No one should doubt that I could swim unassisted from Guam to Hawaii. After all, I can swim 2 miles unassisted, and the trip from Guam to Hawaii (3,950 miles) is simply the cumulative outcome of one 2-mile swim after another.