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.
Seriously? We were discussing saltation in the context of HOX genes, and embryonic development .
There was a very specific argument I was making and Torley more or less admitted the conclusion was that WILD saltation had to happen if one was to reconcile Paul Nelson’s argument with common descent. He even argued that vertebrates were being born off invertebrates at some point!
You NEVER had the balls to address that
How can you possibly be so obtuse? Do you really think symbiogenesis is even remotely as outrageous as invertebrates giving birth to goddamn vertebrates?
And what about common descent? where did I quit?
Unresponsive
You said saltations don’t happen. I offered symbiogenesis. You bailed. You still won’t say whether symbiogenesis is saltational.
No, it’s not
and you did it again, and you know it
And everyone knows that amyl nitrate usage amongst hemophiliacs peaked in the 1980’s.
#alternativefacts
Seriously, though – the effect of IV drug use and MSM as the route of infection have been extensively studied for their effect on the rate of progression to AIDS. They are (minor) factors. But HAART works, in IVDU, in MSM, in hemophiliacs and in the monogamous heterosexual partners of the aforementioned. Why the hell should THAT be the case?
This is grade A crackpottery.
Yes, right there at that post you linked to.
Why not start an OP on it? Do you really think it belongs in a thread on the sea anemone?
LOL, you’re a joke
Mung,
I’d be happy if an admin took PaV’s “These are facts” post, you know, the one where he said the WHO was making shit up for Big Pharma, and made that an OP, and moved all the relevant posts to the new thread.
But you’d probably complain about that, too.
Meh.
LoL. Well, maybe not, since I sanction child abuse, who knows what else I might sanction!
And you’re spending another Friday night with me!
I can’t tell you how happy that makes me.
ok dazz, let me try a different approach.
Scientists discovered an amazing fact. An organism with a highly complex genome, one that goes back to the very Cambrian itself! You would think that this would falsify common descent, but of course, it didn’t.
Perhaps a rabbit in the Cambrian would falsify common descent! Because, finding a genome like this, is like finding a pre-cambrian rabbit.
Now we’re talking… back to my original question:
From the OP:
VJT, I still haven’t seen any defense of this claim. Do you have any evidence that Dr. Hunter thinks these genes were unused? Wouldn’t that mean that he thought they were unused in the sea anemone? Or did you just not think that far ahead?
Oh good. I love recursion!
I don’t think so.
So to sum it up…
Oh… but then later..
Yes, and I provided all the logic that a young dazz could need. Here’s another take on it:
The complexity [or lack thereof] of the earliest known life form tells us absolutely nothing about whether common descent is true or not. Both complexity in early organisms and lack of complexity in early organisms is compatible with common descent.
All evidence available to date indicates that we cannot rely on genome complexity to be an indicator of common descent.
Mung:
Fixed that for you.
We didn’t evolve from chimps, we both evolved from a common ancestor.
So both lineages evolved. If we split about 6 million years ago, and the typical ape-ancestor generation time was about 20 years, that’s 300.000 generations, but for each lineage. So about 600.000 generations in total, if our estimates of generation time and divergence is correct.
What the hell are you even trying to calculate here?
PaV, we know a typical human being probably has over 100 mutations different from it’s parent. Not amino-acid substitutions, but nucleotide differences.
Yes, pretty much. Endosymbiosis is not a genetic mutation. So when you say “they are still bacteria”, you are not saying something that argues against evolution, or which is a surprise to anyone who understands at least some of it.
Just like if you said about fish evolving into tetrapods (or humans and chimps evolving from another ape-like ancestor) “yeah but they’re still just multicellular eukaryotes”, you’re also not saying something of any surprise or interest. It’s a completely uninteresting statement that has no bearing on the factual status of these evolutionary transitions, and it accomplishes nothing in the way of diminishing the results of the long-term evolution experiment. Nobody thinks they’re going to become something other than bacteria, and the truth of evolution isn’t contingent on them becoming something else.
This looks like one of those ridiculous caricatures you guys love to pull.
“Everything is compatible with common descent, LOLOLOL!!!111one”
But anyway.
You seem to (reluctantly?) admit that this does not falsify common descent.
If you think it doesn’t, this can’t be the “genomic equivalent of Haldane’s Precambrian rabbit”… so what the fuck are you doing defending Hunter if you think he’s wrong?
Look, it’s pretty simple. You either buy Hunter’s “Precambrian anemone-rabbit” crap and reject evolution wholesale or you stop supporting him on this nonsense
http://i66.tinypic.com/6hp2sp.jpg
How can we test the claim that humans and chimps share a common ancestor? What account for the anatomical and physiological differences observed? Please show your work. The point being no one has to refute Common Descent if it can’t even be tested
That’s funny, I thought all the statistics were just made up by the WHO and Big Pharma. If so, then those numbers aren’t facts, and there’s nothing to refute.
One wonders how you refute a fact.
Mung has lately taken to defending Frankie. I’d not read too much into it, he’s just a professional troll basically, he’ll do whatever he thinks will rub people up the wrong way just for a laugh.
I wonder! Maybe we could compare genomes. Study the comparative morphology, anatomy, cytology, biochemistry, physiology, and look at the consilience between different methods of comparison. Or we could attribute relatedness to common design because we have an unshiftable prejudice.
Common descent accounts for it.
To you, Joe? Really? Who can only parrot the responses that litter the comment columns here and elsewhere. I’ll say this for you, Joe. You are indefatigable.
Common descent will remain a working hypothesis because it is supported by evidence. It will be rejected if another hypothesis that better explains the observed facts comes along.
ETA:
Evidence of Common descent – an overview
Yeah, Frankie, Sal, johnnyb, Hunter… all YECs. All the while he questions Torley, with whom he is supposed to share some fundamental views like the age of the earth or common descent
I stand by my prediction that he’ll be a YEC before the year ends
…
Hey FrankenJoe, are house cats and tiger related? What is their evolutionary relationship and how can you tell?
Show us your ID-Creationist baraminology science.
I shit you not.
So now in the fantastical theory of evolution common descent explains everything.
I could care less. I accept common descent. No reluctance needed. What I don’t like is VJT misrepresenting Hunter’s argument.
I don’t think Dr. Hunter thinks this falsifies common descent. So if he’s wrong about something in his article no one here has yet managed to point out what it is that he is wrong about, including the author of the OP, who completely missed the point.
Here’s an idea. One of the geniuses here who troll Hunter’s site can go over and ask him if this finding falsifies common decent.
Acartia, I love the pics, keep them coming!
🙂
Mung,
Seems to me you still don’t understand that whether something counts as falsification or not is not a matter of opinion.
Again, Precambrian rabbits would falsify evolution and common descent no matter what you or anyone else thinks . Saying that this is the genomic equivalent to Precambrian rabbits implies that Hunter is claiming that this also falsifies evolution. Of course Hunter is wrong
dazz,
What makes you so smart, exactly?
OMagain,
By proving otherwise. Isn’t that obvious?
And, if the “facts” can’t be budged, then the theory must go. Unless, of course, it’s Darwinism.
Nope. It just explains the nested hierarchy of extant and extinct life on Earth. It’s falsifiable and supported by evidence. There’s no other explanation I know of that doesn’t either explain everything or nothing. “Intelligent Design” varieties tend to do both. That may be the source of your confusion. Have a look at the Wikipedia page I linked to for a few headline examples of the evidence. Dare I suggest Talk Origins too.
Mung,
It can get humorous, can’t it?
Thank you for the changed tone.
I’m in a hurry, so I will be brief, and perhaps make some mistakes.
In the graph you show about the mutations from LTEE, I just looked at it, and there are fewer non-synonomous mutations after 50,000 generations at the beginning.
Now, the first thought would be to say that, aha, we’re dealing with fewer overall replications. However, why all of a sudden all these mutations, early on, and then a tapering off. Did all of these mutations come about almost at once because of a changed environment? IOW, are these “directed” mutations.
That they taper off with time suggests they might be, and the unnecessary mutations are whittled away to correspond to the given environment.
I presume that by “endosymbiosis” you’re talking about mitochondria; but, maybe you’re referring to something else. I don’t know, so, I’ll assume that.
But mitochondria alone aren’t going to provide the move towards multicellular-ity.
And, if this “endosymbiotic” event is the basis of multicellular life, then what prevented it from happening sooner?
That’s one question.
However, since you seem to be admitting that all the mutations in the world aren’t going to get us from one “domain” to the other, then what is it that exists that can provide the “symbiotic” event? Certainly not Archea, right?
So, we’re left with no notion as to how bacterial life began. And, we don’t know how the mover from prokaryote to eukaryote occurred. Mutations won’t explain it. Then what does? Design?
What ancestor was this? Do we find it in the fossil record?
Yes PaV, watching clowns like you and Joe and Mung continually put on the big red nose for us is very entertaining! 🙂
In the case of ID it could be the source of common design.
A constant source of amusement. 🙂
Isn’t that what Chucky D said?
“Both the parent and all the transitional varieties will generally have been exterminated by the very process of formation and perfection of the new form.”
“…new and improved varieties will inevitably supplant and exterminate the older, less improved and intermediate varieties.”
Talk about ad hoccery.
And you folks don’t even understand your own theory.
LOL! Not only is Mung defending Joe G, he’s now channeling Joe G’s idiocy. 😀
http://www.nationalgeographic.org/encyclopedia/speciation/
No. Look at the graph again, it shows small fluctuations in the relative proportions of mutations over the course of the experiment, with the greatest amount of variance from one section to the next, at the beginning.
But it’s not like all the mutations happened at the beginning of the experiment, there’s nothing in the graph that implies that. The different “bars” on the graph correspond to what the distribution was like at the time. At 500 generations, a bit over 50% of the mutations at that time resulted in amino acid substitutions. The number above the bar, 47, is the total number of mutations that had happened at generation 500. But as you can see, mutations keep happening at a relatively steady rate.
Further along, at generation 5000 for example, the total number of mutations had increased to 144. Of those 144 mutations, the number of them resulting in amino acid substitutions had declined slightly to slightly below 50%. As the generations accumulate subsequently, the relative proportions among the types of mutations that happen seem to “settle out” and not fluctuate much any more.
They accumulate as if they are random, and the average distribution crystallizes out as more and more data is accumulated.
In the same way, if you throw a fair coin only 5 times, it might come up HHHHT for example. There’s simply not enough data, not enough throws, to establish whether the coin is fair. So if you only throw it 5 times and you get HHHHT, you might naively take to mean it isn’t a fair coin.
But if you keep throwing the coin, the distribution will settle on 50:50 H/T. That’s the same phenomenon we see at work here. It doesn’t look guided, it looks random.
tesst
Why not?
I don’t claim to know why the circumstances that allowed endosymbiosis to happen, did not happen sooner. Are you going to hide God in that gap now?
I don’t understand the question. “What is it that exists that can provide the symbiotic event?”
One organisms engulfs another, so one now lives inside the other, initially as a parasite, yet later for mutual benefit as they adapt to each other.
This conclusion, even if true, is entirely irrelevant to what we were discussing. I never claimed to know what the origin of life was. We were discussing your several misconceptions and mistaken beliefs about Michael Behe’s work regarding mutations and probabilities.
Yet every time we discover how you didn’t understand something and have made several basic mistakes, you try to change the discussion to something else, barely related.
Yeah we do, it’s endosymbiosis. An archaeon engulfed an alpha-proteobacterium.
No, endosymbiosis. Endosymbiosis is not a mutations, yet that is still the explanation.
Why doesn’t it look like an equilibrium state has been reached?
Those are not mutually exclusive, so I’m not claiming it hasn’t.