Two kinds of complexity: why a sea anemone is not a Precambrian fossil rabbit

The British biologist J.B.S. Haldane is said to have remarked that the discovery of fossil rabbits in the Precambrian would falsify the theory of evolution. Over at Evolution News and Views, Dr. Cornelius Hunter has argued in a recent post that the sea anemone (whose genome turns out to be surprisingly similar to that of vertebrates) is “the genomic equivalent of Haldane’s Precambrian rabbit – a Precambrian genome had, err, all the complexity of species to come hundreds of millions of years later.” Apparently Dr. Hunter is under the impression that many of these ancestral genes would have been lying around unused for much of that time, for he goes on to triumphantly point out that “the idea of foresight is contradictory to evolutionary theory.” RIP, evolution? Not by a long shot.

An unfortunate misunderstanding

Dr. Hunter seems to have missed the whole point of the report that he linked to. A sentence toward the end of the report would have set him right, had he read it more carefully (emphases and square brackets are mine – VJT):

It’s surprising to find such a “high level of genomic complexity in a supposedly primitive animal such as the sea anemone,” [Dr. Eugene V.] Koonin [of the National Center for Biotechnology Information (NCBI) in Bethesda, Md.] told The Scientist. It implies that the ancestral animal “was already extremely highly complex, at least in terms of its genomic organization and regulatory and signal transduction circuits, if not necessarily morphologically.

That’s right. Genomic complexity and morphological complexity are two completely different things. That was the take-home message of the report. It was also the message of the other report cited by Dr. Hunter:

It is commonly believed that complex organisms arose from simple ones. Yet analyses of genomes and of their transcribed genes in various organisms reveal that, as far as protein-coding genes are concerned, the repertoire of a sea anemone — a rather simple, evolutionarily basal animal — is almost as complex as that of a human. (Emphases mine – VJT.)

As if that were not clear enough, Figure 1, on the opening page of the report, spells it out:

Figure 1: Animal miRNAs and morphological complexity. Grimson et al.3 (data along red lines) reveal the evolutionary origin of animal miRNAs by examining organisms at the base of the animal tree. Combining their data with previous work, three different measures of complexity become apparent: the number of protein-coding genes, total number of neurons and number of miRNAs. There is relatively little correlation between morphological complexity and the number and diversity of protein-coding genes. However, miRNA number correlates well with the organism’s total number of neurons. Indeed, a large proportion of vertebrate miRNAs are expressed in the nervous system. These data also show the dynamic nature of the miRNA complement in each lineage, particularly visible in rapidly evolving species (Oikopleura and fruitfly).

Morphologically, the ancestral animal was a very simple creature – so simple that the only real debate going on at present is whether it was more like a comb jelly (a creature with muscles, a nerve net and sensory organs, but no brain or central nervous system, pictured above, image courtesy of Kevin Raskoff) or a sponge (which is sessile and which lacks a nervous system altogether). Certainly it was nothing like as complex as a fly or a worm.

Genetically, however, the ancestral animal seems to have been in some respects better endowed than a fly or a worm. As the report cited by Dr. Hunter puts it (emphases mine – VJT):

The genome of the sea anemone, one of the oldest living animal species on Earth, shares a surprising degree of similarity with the genome of vertebrates, researchers report in this week’s Science. The study also found that these similarities were absent from fruit fly and nematode genomes, contradicting the widely held belief that organisms become more complex through evolution. The findings suggest that the ancestral animal genome was quite complex, and fly and worm genomes lost some of that intricacy as they evolved… The researchers also discovered that exon-intron structure is very similar between modern vertebrates and sea anemones. Both have intron-rich genomes and about 80% of intron locations are conserved between humans and anemones. Fly and nematode genomes, on the other hand, have lost between 50 and 90% of the introns likely present in the animal ancestor.

Building the Precambrian genome – was foresight required?

And what were these genes doing in the original ancestor, anyway? Is there any evidence to suggest that they were placed there in an act of foresight, to be used only by the ancestor’s distant descendants? I’m afraid there isn’t. Dr. Hunter has made an inferential leap here. He isn’t the only one: Dr. Stephen Meyer makes a similar criticism in a 2001 paper which he co-authored with P. A. Nelson and Paul Chien, The Cambrian Explosion: Biology’s Big Bang. Referring to Dr. Susumu Ohno’s now-famous paper, The notion of the Cambrian pananimalia genome (Proceedings of the National Academy of Sciences, Vol. 93, pp. 8475-8478, August 1996), in which Ohno proposed that “all those diverse animals of the early Cambrian period, some 550 million years ago, were endowed with nearly identical genomes, with differential usage of the same set of genes accounting for the extreme diversities of body forms,” Dr. Meyer objects that Dr. Ohno “envisions the pananimalian genome arising well before its expression in individual animals. Specific genes would have arisen well before they were used, needed or functionally advantageous” (pp. 31-32). However, in his paper, Dr. Ohno makes it clear that the ancestral genome he is envisaging was “rather modest in size,” and he points out that all of the five genes which he argues were “certain to have been included in the Cambrian pananimalia genome” were in fact useful to organisms back in the Cambrian period: indeed, it was possession of these genes that “made the Cambrian explosion possible.” Finally, I would like to pass on a rather blunt but factually accurate observation made by Dr. Nick Matzke, in a comment on an Uncommon Descent post I authored back in 2015:

…[B]ecause he’s not a paleontologist, one thing Ohno misses, IIRC, is that there is clear evidence of bilaterians in the Precambrian — trackways and burrows indicating bilateral symmetry, a coelom, etc., and these continually increase in complexity through the small shelly fossils, only reaching the “classic” Cambrian Explosion tens of millions of years later. This is all true regardless of one’s interpretation of the Edicarans etc. Thus, it’s idiotic to say, as Meyer does, that Ohno’s hypothesis means “the pananimalian genome ar[ose] well before its expression in individual animals.” Fossil traces of bilaterians are there before the Explosion, they had worm-level complexity, all of those common genes between all the phyla basically are what is required to specify a bilaterian body plan, which is what worms have.

In a follow-up comment, Dr. Matzke added:

There was, in fact, not a huge amount of origination of genes and proteins required to produce the Cambrian phyla, and we know this because they all have the same basic complement of genes and proteins. The differences that they have are basically due to differential duplication of genes and subsequent modification of genes, and sometimes rearrangement/recombination of pre-existing gene chunks.

A mea culpa

At the time, I was prepared to concede that Dr. Meyer was “probably wrong” on the the question of when these genes and proteins originated, and that they may have arisen long before the Cambrian period. I was even prepared to allow that the genes in the ancestral pan-animalian genome, back in the Precambrian, may have originally had functions of their own, that were later co-opted or ex-apted by their Cambrian descendants, giving rise to new functions. But it seemed to me that Dr. Meyer’s larger point – that the likelihood of even one functional protein fold originating on the primordial Earth was vanishingly low – was still valid. In the end, I thought that Dr. Douglas Axe’s 2010 paper, The Case Against a Darwinian Origin of Protein Folds, clinched the matter, since at least some new protein folds would have had to have come into existence during the Cambrian explosion, even if (as Dr. Matzke pointed out) there were only a few folds that were actually unique to bilaterian animals (the group of animals in which the Cambrian Explosion occurred), with just 17 new domains at the root of bilateria, (sponges and cnidarians having originated earlier).

How wrong I was. Last year, Rumraket wrote an excellent post debunking Dr. Axe’s claim that only about one in 1077 sequences of 150 amino acids was capable of folding and thereby performing some function — any function. There are, at the present time, no good grounds for accepting such a claim, and there are several grounds for treating it with skepticism. In my review (written last year) of Dr. Axe’s book, Undeniable, I describe how my own confidence in the much-vaunted one in 1077 figure was shattered, when I emailed some scientists in the field who kindly set me straight. I would therefore like to offer my belated apologies to Rumraket and to Dr. Matzke. They were right and I was wrong.

If you’re going to argue for design in the genome, this is not the way to do it. Here’s a better way, which doesn’t even use the word “design.” The facts speak for themselves.

Two questions for Dr. Hunter

Finally, I’d like to pose two simple questions to Dr. Hunter, regarding the papers he cited:

(1) Do you agree with the claim that humans are scarcely more complex (genetically speaking) than sea anemones?

(2) Can you cite a single proponent of either Intelligent Design or creationism who predicted this discovery, prior to 2005?

Complexity – good and bad metrics

Regarding (2), I can attest that leading ID proponents fought against the claim, tooth and nail, appealing to the “fact” that human beings have 210 cell types, while Cambrian animals had about 50 and sponges, only 5 (see this paper, for instance), and arguing that new genes and proteins would have been required to generate these additional cell types. However, the oft-repeated assertion that humans have 210 cell types turns out to be a myth, which has been roundly debunked by Professor P.Z. Myers. What’s wrong with this assertion?

The short answer: this number and imaginary trend in cell type complexity are derived entirely from an otherwise obscure and rarely cited 60 year old review paper that contained no original data on the problem; the values are all guesswork, estimates from the number of cell types listed in histology textbooks. That’s it.

And here are the original references cited to back up those figures about the number of “cell types” (a term which has never been explicitly defined) in various kinds of animals (emphases mine – VJT):

5. Andrew, W. 1959. Textbook of Comparative histology. Oxford Univ. Press, London

13. Borradaile, L.A., L.E.S. Eastham, F.A. Potts, & J. T. Saunders. 1941. The Invertebrata: A manual for the use of students. 2nd ed. Cambridge Univ. Press, Cambridge.

85. Maximow, A.A. & W. Bloom. 1940. A textbook of histology. W. B. Saunders Co., Philadelphia.

126. Strasburger, E., L. Jost, H. Schenck, & G. Karsten. 1912. A textbook of botany. 4th English ed. Maximillian & Co. Ltd. London.

Further comment is superfluous.

I’d also like to draw readers’ attention to a 2007 post by Professor Larry Moran, titled, The Deflated Ego Problem, in which he gently pokes fun at scientists who clung to the belief that the complexity of the human genome was far greater than that of “primitive” animals like flies and worms, and listed seven proposals (all invalid, in his view) for redeeming the complexity of the human genome.

Dr. Hunter’s statement that “we repeatedly find early complexity” when investigating the history of animals suggests that he would answer question (1) in the affirmative: our genes are about as complex as a sea anemone’s. As for morphological complexity, I can only state that as far as I can tell, there isn’t any straightforward way of measuring it, although I have no doubt that I’m structurally far more complex than a worm or a sea anemone. (Insects I’m not so sure about – see below.)

I understand that a recent paper in Nature (which unfortunately I cannot access) has finally addressed the origin and evolution of cell types in a rigorous fashion, and that Steven McCarroll’s Lab at Harvard Medical School and the Broad Institute is attempting to map the different kind of cells in the body, using micro-RNA.

I’d like to conclude with a quote from P.Z. Myers’ 2007 post, Step away from that ladder, on the subject of complexity, which is well worth reading (emphases mine – VJT):

I’m fairly familiar with the insect neurodevelopment literature, so when I saw papers saying arthropods only have 50-60 cell types, alarm bells started ringing...

I’m also familiar with some embryonic vertebrate nervous systems, and I can say that they tend to have many more cells in them — but they don’t seem to be as precisely identified at the single cell level as the invertebrate CNS. We have large populations of cells with similar patterns of molecular specification, rather than this kind of precise, cell-by-cell programmatic identity.

Now, from a genetic perspective, which pattern is more complex? I don’t know. They’re both complex but in very different ways — it’s basically impossible at this point to even identify a quantifiable metric that would tell us how complex either of these kinds of systems are. How many cell types are present in this whole animal? I don’t know that either… I bet it’s many more than 60, though.

I’ll go out on a limb and make a prediction: any difference in the degree of complexity, assuming an objective method of measurement, in the triploblastic metazoa [basically, all animals except sponges, placozoans, cnidaria and possibly comb jellies – VJT] will much be less than an order of magnitude, and that the vertebrates will all be roughly equivalent… and that if any group within the vertebrates shows a significant increase in genetic complexity above the others, it will be the teleosts. I’ll also predict that any ‘extra’ complexity in members of these groups will not be a significant factor in their fitness, although it might contribute to evolvability.

What do readers think? Over to you.

319 thoughts on “Two kinds of complexity: why a sea anemone is not a Precambrian fossil rabbit

  1. No one was saying that finding a rabbit in the Precambrian would be surprising (problematic, at least) because of its complexity. It’s the matter of evolutionary limitations, the fact that land-adapted rabbits wouldn’t evolve from worms or trilobites out of the blue without some kind of fossil “progression” being visible. There simply is a lot of evolution necessary to get from early chordates, even early vertebrates, to bunnies hopping around and eating angiosperms.

    That “complexity” (functional complexity, generally) is brought up constantly by IDists doesn’t change the fact that it is simply the case that evolution may produce highly complex organisms, often more complex than necessary due to old development steps not being easily lost. Hunter’s fantasy that ID claims are meaningful aren’t impressive to anyone who hasn’t already bought into such baseless assertions.

    It’s a strawman argument, although I don’t have any reason to suppose that Hunter knows any better. But if he’s going to weigh in on the matter, he should.

    Glen Davidson

  2. However, miRNA number correlates well with the organism’s total number of neurons.

    I’d be a bit more cautious. This figure seems suspiciously like a dog’s ass plot. The sample is small and highly biased. But at least “number of neurons” is quantifiable, unlike morphological complexity. What this needs is an analysis using independent contrasts (to remove the bias of phylogeny), a much larger and unbiased sample size, and perhaps controlling for body size and genome size.

  3. vjt:

    If you think that rumraket destroyed Axe’s argument, then you are mistaken.

    Darwinists, as they cackled among themselves, gave argument after argument that Behe and Snoke’s calculations were completely wrong. According to their calculation, the probability of even a simple two amino acid change coming about randomly was incredibly, incredibly low. All those arguments. Behe was wrong. They knew it. Just look here; just look there.

    And what did Behe do? He looked for a way to test the results of his computer simulation. He settled on the malarial parasite. And, guess what: the probability of even a two-amino acid substitution turned out to be extremely low, demolishing all the arguments the Darwinists made regarding his numbers and his results.

    vjt: you’re going down the wrong road. It’s not too late.

  4. Glen Davidson:

    Pseudoscience on display:

    That “complexity” (functional complexity, generally) is brought up constantly by IDists doesn’t change the fact that it is simply the case that evolution may produce highly complex organisms, often more complex than necessary due to old development steps not being easily lost. Hunter’s fantasy that ID claims are meaningful aren’t impressive to anyone who hasn’t already bought into such baseless assertions.

    This is what pseudoscience looks like: that which would prove our position is, unfortunately, beyond experimental verification. Nevertheless, we believe X,Y, or Z to be true.

    Always excuses; never an acceptance of what is “actually seen” implies—which, of course, is how real science operates.

  5. PaV:
    And what did Behe do?He looked for a way to test the results of his computer simulation.He settled on the malarial parasite.And, guess what: the probability of even a two-amino acid substitution turned out to be extremely low, demolishing all the arguments the Darwinists made regarding his numbers and his results.

    I wonder if you understand what you are copying. You seem to have swallowed the argument that ONE organism experiencing ONE specific change is highly unlikely, THEREFORE ANY (of countless trillions) of organisms experiencing ANY useful two amino acid substitutions must be equally small.

    This the argument that if you toss a ball up in the air, then since the probability of it coming down precisely HERE is very small, therefore the probability of it coming down AT ALL is equally small. Yet Behe and Axe keep repeating this silly notion, and their copyists (those who are creationists) keep ignoring the basic problems with it.

    Nobody doubts Behe’s calculations, and no non-creationist fails to realize their irrelevance to real world biology.

  6. PaV: Always excuses; never an acceptance of what is “actually seen” implies—which, of course, is how real science operates.

    Golly, I try to keep abreast of these things somewhat, but I was not aware that someone had actually seen a rabbit in the pre-Cambrian. Do you have a link to this?

  7. PaV:
    Glen Davidson:

    Pseudoscience on display:

    This is what pseudoscience looks like: that which would prove our position is, unfortunately, beyond experimental verification.Nevertheless, we believe X,Y, or Z to be true.

    Always excuses; never an acceptance of what is “actually seen” implies—which, of course, is how real science operates.

    Oh yeah, you can just see “design” in life without actually showing intelligent choice, but we can’t reliably observe developmental pathways that served a different function yet are modified at some point to serve another one.

    The bones of bird wings are a fine example of the latter. The bones that would become articulated in the forelimbs of theropods develop as separate bones yet today, then they fuse into the rigid structures that serve avian flight. It isn’t experimental data, but it’s the scammers and pseudoscientists who think that only that counts, while astronomers and geologists know otherwise (some experimental data exist in both, but huge numbers of phenomena will never be replicated as such experimentally).

    You fail on all accounts, whether in knowing what science is, and in the good evidence we have for useless complexity, while your mindless beliefs have neither good observational data nor good experimental data.

    The BS from your side is never-ending.

    Glen Davidson

  8. PaV:

    And what did Behe do?He looked for a way to test the results of his computer simulation.He settled on the malarial parasite.And, guess what: the probability of even a two-amino acid substitution turned out to be extremely low, demolishing all the arguments the Darwinists made regarding his numbers and his results.

    And what did science do? Science looked at dozens of real world cases where the actual results Behe said were impossible actually happened, meaning Behe’s made up “it’s too improbable therefore GAWDDIDIT!” calculations were worthless. Behe remains the laughingstock he’s been since Kitzmiller v. Dover.

  9. GlenDavidson: Oh yeah, you can just see “design” in life without actually showing intelligent choice, but we can’t reliably observe developmental pathways that served a different function yet are modified at some point to serve another one.

    That doesn’t mean blind and mindless processes didit, Glen.

    The BS from your side is never-ending.

    And the projection from your side is never ending

  10. Hey PaV, could you write up an OP sometime explaining how, just like evolution and global warming, the scientific community is lying to us about HIV? Some of us are very curious to know your thoughts on the matter.

  11. Genomic complexity and morphological complexity are two completely different things.

    I have to ask, so what? What makes you think Haldane’s rabbit was chosen because of its complexity?

    Why this sudden concentration on minutiae while missing the main point. Do you have any plans to address Hunter’s points about theory protectionism and naïve falsificationism?

    Oh, and here’s a relevant quote from Hunter which you seem to have overlooked:

    Consider, for example, the genome of the starlet sea anemone, Nematostella vectensis.

    And here he is quoting the same part you did:

    It implies that the ancestral animal “was already extremely highly complex, at least in terms of its genomic organization and regulatory and signal transduction circuits, if not necessarily morphologically.

  12. And what were these genes doing in the original ancestor, anyway? Is there any evidence to suggest that they were placed there in an act of foresight, to be used only by the ancestor’s distant descendants? I’m afraid there isn’t. Dr. Hunter has made an inferential leap here.

    See that part on bold there? Did that come from something Dr. Hunter wrote?

    Here’s Dr. Hunter’s actual words:

    In other words, it was the genomic equivalent of Haldane’s Precambrian rabbit — a Precambrian genome had, err, all the complexity of species to come hundreds of millions of years later. In other cases it has more complexity than species such as worms and flies, which, according to evolution, must have lost enormous amounts of genetic complexity.

    So first, he doesn’t say what you represent him as saying. Second, you left out a relevant part of what he did say.

  13. petrushka:
    Behe’s calcs are the poster child for bumblebees can’t fly engineering analysis.

    Except they weren’t Behe’s calcs. As Behe says the numbers are from a peer-reviewed paper on Antimalarial drug resistance– Prevention of resistance by antimalarial combination therapy:

    The theory underlying combination drug treatment of tuberculosis, leprosy, and HIV infection is well known and is now generally accepted for malaria (5, 8, 55–58). If two drugs are used with different modes of action, and therefore different resistance mechanisms, then the per-parasite probability of developing resistance to both drugs is the product of their individual per-parasite probabilities. This is particularly powerful in malaria, because there are only about 10^17 malaria parasites in the entire world. For example, if the per-parasite probabilities of developing resistance to drug A and drug B are both 1 in 10^12, then a simultaneously resistant mutant will arise spontaneously every 1 in 10^24 parasites. As there is a cumulative total of less than 10^20 malaria parasites in existence in one year, such a simultaneously resistant parasite would arise spontaneously roughly once every 10,000 years — provided the drugs always confronted the parasites in combination. Thus the lower the de novo per-parasite probability of developing resistance, the greater the delay in the emergence of resistance.

    This one is becoming a PRATT

  14. Mung Do you have any plans to address Hunter’s points about theory protectionism and naïve falsificationism?

    Corny didn’t make any points about theory protectionism and naïve falsificationism. As per usual he asserted another bunch of Creationist bullshit backed with the usual misrepresentations of the scientific literature and outright lies.

    It is pretty funny that you’ve now appointed yourself guardian of the hopelessly inept and willfully dishonest Creationists like Corny and Joe. I’m sure they appreciate your skillful help. 🙂

  15. Wow. The more I re-read Hunter’s article the more I see how badly he’s been misrepresented.

  16. Mung:
    Wow. The more I re-read Hunter’s article the more I see how badly he misrepresented science

    Fixed it for you Mung.

  17. And what were these genes doing in the original ancestor, anyway? Is there any evidence to suggest that they were placed there in an act of foresight, to be used only by the ancestor’s distant descendants? I’m afraid there isn’t. Dr. Hunter has made an inferential leap here.

    This makes it seem like Dr. Hunter claimed these genes were placed there in act of foresight. Yet he never claimed any such thing, nor did he claim there was evidence for such a claim. VJT has given us a prime example of a straw-man argument.

    Perhaps he’s spent too much time here at TSZ without the proper inoculations.

  18. Mung: This makes it seem like Dr. Hunter claimedthese genes were placed there in act of foresight. .

    That’s exactly what he did imply. From Hunter’s article :

    “The lead author of the sea anemone study explained, “We have this basic toolkit now for the whole animal kingdom.” Of course the idea of foresight is contradictory to evolutionary theory.

    Amazing how far over backwards one Liar for Jesus will bend to defend another Liar for Jesus.

  19. Mung: This makes it seem like Dr. Hunter claimed these genes were placed there in act of foresight. Yet he never claimed any such thing, nor did he claim there was evidence for such a claim. VJT has given us a prime example of a straw-man argument

    Generally Dr Hunter makes no claims at all, but uses the ” people say” technique

  20. PaV: If you think that rumraket destroyed Axe’s argument, then you are mistaken.

    Okay. Why?

    Darwinists, as they cackled among themselves, gave argument after argument that Behe and Snoke’s calculations were completely wrong. According to their calculation, the probability of even a simple two amino acid change coming about randomly was incredibly, incredibly low.

    Yet it happens all the time. From the Long Term Evolution Experiment with E coli:
    empo and mode of genome evolution in a 50,000-generation experiment.
    Tenaillon O, Barrick JE, Ribeck N, Deatherage DE, Blanchard JL, Dasgupta A, Wu GC, Wielgoss S, Cruveiller S, Médigue C, Schneider D, Lenski

    RE.
    Abstract
    Adaptation by natural selection depends on the rates, effects and interactions of many mutations, making it difficult to determine what proportion of mutations in an evolving lineage are beneficial. Here we analysed 264 complete genomes from 12 Escherichia coli populations to characterize their dynamics over 50,000 generations. The populations that retained the ancestral mutation rate support a model in which most fixed mutations are beneficial, the fraction of beneficial mutations declines as fitness rises, and neutral mutations accumulate at a constant rate. We also compared these populations to mutation-accumulation lines evolved under a bottlenecking regime that minimizes selection. Nonsynonymous mutations, intergenic mutations, insertions and deletions are overrepresented in the long-term populations, further supporting the inference that most mutations that reached high frequency were favoured by selection. These results illuminate the shifting balance of forces that govern genome evolution in populations adapting to a new environment.

    So about 450 mutations have accumulated in a lineage. The red piece of the bar is non-synonymous mutations, meaning they are mutations that caused amino acid changes in a protein coding genes. Roughly 50% of mutations over the course of the experiment, caused amino acid changes. That would be about 225 amino acid substitutions that have accumulated over 50.000 generations.

    What use is Behe’s probability calculations then?

  21. PaV: And what did Behe do? He looked for a way to test the results of his computer simulation.

    His computer simulation? What computer simulation?

    He settled on the malarial parasite. And, guess what: the probability of even a two-amino acid substitution turned out to be extremely low

    Yet roughly 225 accumulated in about 20 years in the LTEE.

    Two hundred and twenty five.

  22. PaV,

    He settled on the malarial parasite. And, guess what: the probability of even a two-amino acid substitution turned out to be extremely low, demolishing all the arguments the Darwinists made regarding his numbers and his results.

    How’s that work? He calculated a probability, which demolishes all subsequent arguments against his probability calculation?

    His method is awful. Simple, but awful.

  23. Ladies and gentlemen… ID theory in a nut shell:

    If you’re going to argue for design in the genome, this is not the way to do it. Here’s a better way [enter James “we know nothing, nothing, nothing” Tour], which doesn’t even use the word “design.”

    facepalm

    Is this how trained philosophers think?

  24. Hi Mung,

    Thank you for your comments. You ask:

    Do you have any plans to address Hunter’s points about theory protectionism and naïve falsificationism?

    I didn’t address them in my OP because they didn’t interest me very much. I happen to share Richard Dawkins’ opinion that fossil rabbits in the Precambrian really would falsify evolution. In his post, Dr. Hunter disparagingly refers to “naïve falsificationism — the thinking that a single finding is going to take down a theory so deeply imbedded in our thinking,” and I must admit that if I found a single fossil rabbit in Precambrian strata, I’d probably think it had somehow been washed into those strata by mistake – rather like the case of a Miocene Homo sapiens found in 1812 (Guadeloupe woman). But if I found Precambrian fossil rabbits in several widely scattered areas, that alone would be enough to overturn the theory for me. I wouldn’t go asking for Precambrian human skeletons as well.

    Dr. Hunter complains about “theory protectionism,” or “erecting insurmountable protective barriers around a theory.” Insurmountable, my foot! Any young-earth creationist will tell you that plants and animals were all made within a week, and many YECs date Global Flood strata from the Cambrian to the end of the Cretaceous. These people would expect to find Cambrian fossil rabbits, if not Precambrian ones. Dr. Hunter wryly observes: “The fossil record was sufficiently understood in Haldane’s day to know that such as finding was highly unlikely.” “Highly unlikely” only if you make uniformitarian assumptions – which is begging the question. I don’t think Haldane was setting the bar too high, although I do think evolution could be easily falsified in many other ways.

    You also ask:

    What makes you think Haldane’s rabbit was chosen because of its complexity?

    I never said it was. It was Dr. Hunter who said that the complexity of the ancestral animal genome was “the genomic equivalent of Haldane’s Precambrian rabbit.” His term, not mine.

    Dr. Hunter writes that this discovery implies that the ancestral animal “was already extremely highly complex, at least in terms of its genomic organization and regulatory and signal transduction circuits, if not necessarily morphologically.” Here he’s quoting from the report, as you correctly point out. But he didn’t put the last part in emphases, like I did, and I think he missed its significance. Why do I think that? Because of his careless remarks elsewhere in his OP.

    For instance, he writes that the ancestral animal “more complexity than species such as worms and flies,” without taking care to distinguish genetic from morphological complexity. What he should have said was that the genome of the ancestral animal had some genes which worms and flies have since lost, despite the fact that worms and flies are anatomically far more complex than the ancestral animal. He should also have added that worms and insects have gained some genes as well, as the ancestral animal genome would have been fairly small. In short, it’s the lack of nuance in Dr. Hunter’s remarks that makes me wonder if he really understood what he was reading.

    I hope that answers some of your questions.

  25. Allan Miller:
    PaV,

    How’s that work? He calculated a probability, which demolishes all subsequent arguments against his probability calculation?

    His method is awful. Simple, but awful.

    LoL! Behe’s numbers came from a peer-reviewed paper on Antimalarial drug resistance. Your comments are awful. Simple, but awful.

    Why do evolutionists knee jerk when IDists write something? Is it too much to ask to actually check the SOURCE?

  26. Mung: This makes it seem like Dr. Hunter claimed these genes were placed there in act of foresight. Yet he never claimed any such thing, nor did he claim there was evidence for such a claim.

    You are correct. He just asserted that they couldn’t have arisen through evolution. What does that leave? Remember, we are talking about a guy who claims that because scientist often use language that is commonly used do describe acts of intention (eg., coopted) that evolution is intelligently driven.

  27. Lenski’s experiment as support for blind and mindless processes is question begging at best. Or equivocation at worst.

    How was it determined that a blind and mindless process took the only gene that codes for a citrate transport protein, duplicated it and put it under the control of an existing promoter that was on in the presence of O2? Show your work

  28. vjtorley,

    Vincent, have you asked Barry to delete or retract the articles you authored at UD critizing Mikkel now that you admit you were wrong in that regard?

  29. Frankie: How was it determined that a blind and mindless process took the only gene that codes for a citrate transport protein, duplicated it and put it under the control of an existing promoter that was on in the presence of O2? Show your work

    Feel free to present an alternate mechanism, test it and provide the data.

  30. Hi PaV,

    Thank you for your post. Allow me to quote from an ENV post by Casey Luskin (“Problem 3: Step-by-Step Random Mutations Cannot Generate the Genetic Information Needed for Irreducible Complexity,” January 12, 2015):

    Proteins commonly interact with other molecules through a “hand-in-glove” fit, but these interactions often require multiple amino acids to be ‘just right’ before they occur. In 2004, Behe, along with University of Pittsburgh physicist David Snoke, simulated the Darwinian evolution of such protein-protein interactions. Behe and Snoke’s calculations found that for multicellular organisms, evolving a simple protein-protein interaction which required two or more mutations in order to function would probably require more organisms and generations than would be available over the entire history of the Earth. They concluded that “the mechanism of gene duplication and point mutation alone would be ineffective…because few multicellular species reach the required population sizes.”38

    Four years later during an attempt to refute Behe’s arguments, Cornell biologists Rick Durrett and Deena Schmidt ended up begrudgingly confirming he was basically correct. After calculating the likelihood of two simultaneous mutations arising via Darwinian evolution in a population of humans, they found that such an event “would take > 100 million years.” Given that humans diverged from their supposed common ancestor with chimpanzees only 6 million years ago, they granted that such mutational events are “very unlikely to occur on a reasonable timescale.”39

    I refuted this in my review of Dr. Axe’s book, Undeniable, when I wrote:

    In a 2012 ENV post discussing the alleged transition from ape-like creatures to humans, Axe cites a 2008 paper by Durrett and Schmidt, and comments: “Any aspect of the transition that requires two or more mutations to act in combination in order to increase fitness would take way too long (>100 million years).” Here’s my question for Dr. Axe: can you identify a single case in the line leading to human beings, where two or more mutations had to act in combination, in order to confer an increase in fitness in our ancestors? No? So much for Durrett and Schmidt, then.

    Until someone can answer that challenge, I will assume that my argument works against Behe and Snoke as well.

  31. vjtorley: Here’s my question for Dr. Axe: can you identify a single case in the line leading to human beings, where two or more mutations had to act in combination, in order to confer an increase in fitness in our ancestors?

    Absolutely- the generation of new opsins that would require new binding sites and just-so mutations t6hat would tune the new opsins.

    That said can YOU show that just any ole mutations will do the trick? No? So much for your argument, then.

  32. Acartia: He [Dr. Hunter] just asserted that they couldn’t have arisen through evolution.

    Is this something he wrote in his article, because I don’t remember seeing it.

    Please provide the quote.

  33. vjtorley: In short, it’s the lack of nuance in Dr. Hunter’s remarks that makes me wonder if he really understood what he was reading.

    All Dr. Hunter was ever talking about was genetic complexity. I fail to see how you could miss that.

    Consider, for example, the genome of the starlet sea anemone…

    In other words, it was the genomic equivalent of Haldane’s Precambrian rabbit — a Precambrian genome had, err, all the complexity of species to come hundreds of millions of years later. In other cases it [the genome] has more complexity than species such as worms and flies, which, according to evolution, must have lost enormous amounts of genetic complexity.

    The lead author of the sea anemone study explained, “We have this basic [genetic] toolkit now for the whole animal kingdom.” Of course the idea of foresight is contradictory to evolutionary theory. As one evolutionist admitted, it is surprising to find such a “high level of genomic complexity in a supposedly primitive animal such as the sea anemone.” It implies that the ancestral animal “was already extremely highly complex, at least in terms of its genomic organization and regulatory and signal transduction circuits, if not necessarily morphologically.”

    It’s the lack of nuance in you remarks that makes me wonder if you really understood what you were reading.

  34. dazz: the genomic equivalent of Haldane’s Precambrian rabbit would falsify common descent, right Mung?

    I don’t think so.

  35. The existence of rabbits falsifies evolutionism. The existence of genomes falsifies evolutionism. That is because evolutionism cannot account for either.

  36. dazz: why not? Precambrian rabbits would. Why not the genomic “equivalent?

    I don’t agree with your premise. I also don’t think a precambrian rabbit would falsify common descent.

    Try to follow this dazz,

    Imagine an Ur-Organism created by some Deity from which all other organisms descended. How would finding that Ur-Organism falsify common descent?

    If scientists found evidence that the LUCA was highly complex genetically, basically containing all that was needed for subsequent species to evolve from it, that would not falsify common descent. It might require a miracle at the origin of life, but it would not falsify common descent.

  37. Flint,

    Flint: Nobody doubts Behe’s calculations, and no non-creationist fails to realize their irrelevance to real world biology.

    There’s a little problem here, Flint. If, as your comment declares, no “non-creationist” fails to see the irrelevance, then why did they argue against it? Why not simply ignore it? Or, were they threatened?

    Try to be logical.

  38. Flint: I wonder if you understand what you are copying. You seem to have swallowed the argument that ONE organism experiencing ONE specific change is highly unlikely, THEREFORE ANY (of countless trillions) of organisms experiencing ANY useful two amino acid substitutions must be equally small.

    You display your hostility by starting out with a sneering comment. People who are open to the truth are not hostile.

    What about this argument “that ONE organism experiencing ONE specific change is highly unlikely, therefore…..” This statement of yours betrays the fact that you have neither read Behe’s book—while knowing exactly why it is wrong, nor have you even digested the argument he makes through second-hand sources.

    Behe uses Dr. Miller’s number of 1 in 10^20 for malarial resistance to chloroquine. It is a number that starts with each “individual” malarial parasite–which replicates over and over again within the host–reaching a population size of replicates of around 10^12, and then counting the number of persons contacting malaria each year, times the number of years it took for CR to develop.

    This number, and this process, are not typical population genetics type numbers and processes, and the CCC that Behe postulates is impervious to your statement. Simple as that.

  39. PaV: People who are open to the truth are not hostile.

    😀

    The list of hostile people here at TSZ is rather extensive.

  40. Mung: I don’t agree with your premise. I also don’t think a precambrian rabbit would falsify common descent.

    It’s not a premise. It’s not a matter of opinion: how would you fit a Precambrian rabbit in the tree of life? It simply doesn’t work.

    Mung: Try to follow this dazz,

    Imagine an Ur-Organism created by some Deity from which all other organisms descended. How would finding that Ur-Organism falsify common descent?

    WTF? If all organisms descend from a single Ur-Organism, THAT’S UNIVERSAL COMMON DESCENT, regardless of how this Ur-Organisms came to be.

    Mung: If scientists found evidence that the LUCA was highly complex genetically, basically containing all that was needed for subsequent species to evolve from it, that would not falsify common descent. It might require a miracle at the origin of life, but it would not falsify common descent.

    LUCA didn’t have to, and almost sure it wasn’t the first living thing on earth, or even the only living thing in existence! You can’t possibly tell me you’ve never heard this!

  41. PaV:
    Flint,

    There’s a little problem here, Flint.If, as your comment declares, no “non-creationist” fails to see the irrelevance, then why did they argue against it?Why not simply ignore it?Or, were they threatened?

    Try to be logical.

    I would also argue against HIV deniers, astrology and bible literalists. That doesn’t make any of those issues relevant.

  42. Mung:

    The list of hostile people here at TSZ is rather extensive.

    FrankenJoe, Phoodoo and bad Mung is a fairly short list WJM does not drop by much anymore.

  43. “Imagine an Ur-Organism created by some Deity from which all other organisms descended. How would finding that Ur-Organism falsify common descent?”

    “WTF? If all organisms descend from a single Ur-Organism, THAT’S UNIVERSAL COMMON DESCENT, regardless of how this Ur-Organisms came to be.”

    LOL

  44. vjtorley: Here’s my question for Dr. Axe: can you identify a single case in the line leading to human beings, where two or more mutations had to act in combination, in order to confer an increase in fitness in our ancestors? No? So much for Durrett and Schmidt, then.

    Here’s a quote from their paper:

    Multiplying
    by 0.75 reduces the mean waiting time to 162 million years, still a very long time. Our previous work has shown that, in humans, a new transcription factor binding site can be created by a single mutation in an average of 60,000 years, but, as our new results show, a coordinated pair of mutations that first inactivates a binding site and then creates a new one is very unlikely to occur on a reasonable timescale.

    To be precise, the last argument shows that it takes a long time to wait for two prespecified mutations with the indicated probabilities.

    So, clearly, for TWO mutations to occur simultaneously, is highly improbable, yes?

    Now, they criticize Behe’s methodology, and his numbers. They write:

    Taking 2N =10^6 and m1 = m2 = 10^-9, Theorem 1 predicts a waiting time of 31.6 million generations for one prespecified pair of mutations in one species . . .

    Wow, what a great improvement!

    What this means is that if there is anything in any of the phenotypic changes between chimps and humans requires TWO mutation to simultaneously appear, then evolution–specifically here, random drift—cannot bring it about, and cannot be proposed as a realistic mechanism which explains chimp/human evolution.

    Your response to this, Vincent, is to challenge Axe to find something that absolutely needs two concomitant mutations.

    (Now, this, in itself, is a bit silly if we consider the malarial parasite. It’s in a ‘life-and-death’ struggle, and yet it requires 10^20 replications to find an answer. It is obvious it needs two mutations simultaneously, otherwise, one mutation would be immediately found by the parasite in the run-up to a trillion copies of itself inside the host. So, your argument assumes that malarial parasites are in someway more complicated than humans. Really?)

    But, lets turn this around.

    Vincent, your challenge to Axe is to “identify” one single instance where two mutations had to act in combination to confer an increase in fitness.

    Well, Vincent, let’s say your right. Let’s say that every increase in fitness requires only one mutation, and that neutral drift provides all the needed mutations along the way; well, then, given the time span needed for chimps to become humans, then why hasn’t the same process been on-going, and why don’t we see “intermediate” forms?

    How do you turn-off neutral drift? Humans number in the billions. How many individual forms of chimps are there that exist planet wide? Who’s more fit, we who go to Safeway to buy any food we like, or the chimps in the trees? And, if humans are more “fit,” then what is stopping neutral drift from acting?

    Do have any ideas?

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