Right of Reply: Our Response to Jerry Coyne
I would like to fasten on one serious misunderstanding of evolution contained in that response. This:
" The average longevity of marine invertebrate species is 5-10 million years. This is standard evolutionary biology. Thus, the transition from an assumed worm-like ancestor to all of the Cambrian animal phyla took place during the lifespan of, at most, a few successive species."
This makes the implicit assumption of anaagenesis, i.e. that a species originates by the transformation of an ancestral species and ends in the transformation to a descendant species, i.e. that species are lined up nose to tail like a string of sausages. Sorry, but that isn’t how it works. Species can split at any time or, in fact, many times, and each time one or more of the splits may retain the ancestral morphology. Or not. The rate of evolutionary change is not limited by the lifetimes of morphospecies. Further, whenever evolutionary rates have been measured in the fossil record, they have been orders of magnitude slower than the rates of observed evolution in the present day.
There are many other problems, but that one will do for now.
The average longevity of marine invertebrate species is 5-10 million years. This is standard evolutionary biology. Thus, the transition from an assumed worm-like ancestor to all of the Cambrian animal phyla took place during the lifespan of, at most, a few successive species.
This is incredibly fallacious. The fact that the average marine invertebrate species persists in the fossil record for 5-10 million years does not mean that the Cambrian explosion must have consisted of on the order of 2 or 3 successive species. The fact that Bechly either wrote or signed off on that paragraph is amazing, a sign of the depths he’s willing to plumb in order to defend ID. Same goes for when similar numbers are cited for the evolution of whales.
The whales? And in twelve million years? Not likely. The available window of time for the transition from the terrestrial pakicetids to fully marine basilosaurids (Pelagiceti) is only 4.5 million years.
Where’s the citation for this time, and am I going to have to explain why it’s fallacious to simply subtract the age of the oldest basilosaurid from the youngest pakicetid in calculating the window of time available for the terrestrial to aquatic transition?
The emergence of a single pair of coordinated mutations in the human lineage required a waiting time of 216 million years. The separation of the chimpanzee and human lineages took place only six or seven million years ago. These figures are clearly in conflict. This is the standard view, the one held by mainstream evolutionary biologists.
This paragraph implies that it’s a mainstream view that there is a conflict between these “waiting time” calculations and evolutionary timescales, which is obviously not true. Again, sloppy.
If the Cambrian Explosion cannot be contained by a play on words, perhaps it may be constrained by a sleight of hand? The very concept of an explosion, Coyne argues, “is disappearing, with paleontologists increasingly speaking of a ‘Cambrian diversification’.” Are they? Are they really? A search on Google Scholar for academic publications between 2000 and 2019 yields 13,400 matches for the term ‘Cambrian Explosion’ but only 392 matches for ‘Cambrian Diversification.’ The Cambrian Explosion continues to explode: “Evidence is converging,” paleontologists have written recently, “towards picturing the Cambrian explosion as even swifter than what we thought.” This does not look like a disappearing concept at all. Some scholars should leave sleights of hand alone.
Ironically, one of the papers cited later in the article, Daley et al. 2018, concludes by saying:
The fossil record of euarthropods provides our most complete view of the origin and radiation of a major phylum during the Cambrian explosion. Rather than being a sudden event, this diversification unfolded gradually over the ∼40 million years of the lower to middle Cambrian, with no evidence of a deep Precambrian history.
This is a good example of the fact that “cambrian explosion” is likely to remain in use even as evidence accumulates that it may actually have been quite gradual. Simply doing a keyword search isn’t a good indictor of how the event is viewed by researchers in the field.
Coyne is unpersuaded, maintaining that, yes, we have found Ediacaran “animals that appear to be arthropods, muscle-clad cnidarians (the group that includes modern jellyfish and anemones), echinoderms, mollusks, and probable sponges.”
This is pure fantasy. Coyne is unacquainted with the facts. There are no Ediacaran arthropods.
That’s a pretty confident claim. As Coyne said, there are animals that appear to be arthropods, such as Parvancorina. They may very well not be, and I think it’s fair to say that Coyne may be overstating his case for Ediacaran arthropods, but I’d expect a more nuanced response than “pure fantasy”.
There are no Ediacaran echinoderms either. Akarua adami, it is true, was initially attributed to the echinoderms. But apart from pentaradial symmetry, Akarua adami lack all of the synapomorphic characteristics of the echinoderms. The Cambrian fossil record contains stem echinoderms in helicoplacoids and homalozoans (carpoids) after all; and we know from reconstructed phylogenetic trees that pentaradial symmetry does not belong to their ground plan.
Once again, there is uncertainty here - neither Coyne or you guys should be claiming certainty one way or the other.
Some time ago, paleontologists tried to explain the absence of soft-bodied ancestors in pre-Cambrian sediments as artifacts of preservation. No longer. This hypothesis has been refuted by evidence from fossil sites of the Burgess Shale type in Mongolia and China. They yielded nothing but fossil algae.
Contrary to this dismissive hand-wave, the actual papers cited, especially Yuan et al. 2011, discuss some fossils of uncertain phylogenetic affinity that might represent soft-bodied animals. It’s also dishonest to say that palaeontologists no longer try to explain the absence of soft-bodied ancestors in pre-Cambrian strata as the result of preservation bias. Just because you guys have decided this hypothesis has been falsified, doesn’t mean most palaeontologists have.
The last has long been considered by paleontologists as “one of the strongest cases for anagenesis in the fossil record.” Unfortunately, it has just been overturned by the discovery of a new hominin skull that documents the temporal overlap of both species.
The new scientist article cited actually points out that “Anthropologists are conflicted on this point. Spoor says that this suggestion is probably right, but that the evidence against anagenesis is not yet conclusive.”
These are just some of the errors that jumped out at me on the subject of palaeontology, which isn’t really my wheelhouse. I’ve no doubt there will be many more problems with the next 2 parts.
What’s worse, this is the average waiting time for two pre-specified mutations. Not just any two mutations.
Hey Brian, why are you repeating previous falsehoods in your response to Jerry Coyne? You repeat the falsehood that accumulating mutations in proteins inevitably destabilize them, and cite the work of Dan Tawfik to substantiate that point:
Recent work by Weizmann Institute protein scientist Dan Tawfik has reinforced this conclusion. Tawfik’s work shows that as mutations to functional protein sequences accumulate, the folds of those proteins become progressively more thermodynamically and structurally unstable. Typically, 15 or fewer mutations will completely destroy the stability of known protein folds of average size.
Did he actually look at the scientific evidence? My impression is that only read Discovery Institute publications, and accepted their claims uncritically.
it will be interesting to check out how much time require to evolve a biological system by say 1000 small steps. if any step add about 0.1% of survivability how much time it will take to be fixed in the population?
Recent work by Weizmann Institute protein scientist Dan Tawfik has reinforced this conclusion. Tawfik’s work shows that as mutations to functional protein sequences accumulate, the folds of those proteins become progressively more thermodynamically and structurally unstable. Typically, 15 or fewer mutations will completely destroy the stability of known protein folds of average size. Yet, generating (or finding) a new protein fold requires far more amino acid sequence changes than that.
By the way, there’s another problem with this statement. Biologists generally don’t claim that one protein fold evolved into a completely different one by this kind of accumulation of point mutations. Rather, proteins with novel folds are either thought to result from recombinations and fusions of smaller sections of already existing proteins, or de novo from non-coding DNA. This idea that one protein with a unique fold needs to transition gradually by point mutations into another protein with a completely distinct fold is a straw-man.
And then there’s this gibberish:
Finally, calculations based on Tawfik’s work confirm and extend the applicability of Axe’s original measure of the rarity of protein folds. These calculations confirm that the measure of rarity that Axe determined for the protein he studied is actually representative of the rarity for large classes of other globular proteins.
This is another demonstrable falsehood. No reference is given to substantiate the claim that anything in Tawfik’s work somehow supports or extends Axe’s numbers. That’s because no such reference exists. It’s flat out false to claim so.
The falsehoods continue:
The archipelago of functional proteins remains what it has always been: an isolated series of island-like points in a vast sea of possibilities.
The link is to a talk given by Dan Tawfik. But Tawfik is talking about fold-based protein superfamilies. What Tawfik actually states in the talk is that it is not known whether the individual and different folds on which distinct protein superfamilies are classified and based, are mutually related to each other, because neither the sequences nor structures can be aligned. So these superfamilies look isolated from each other in sequence/structure space. Which they very well might be. Hence nobody thinks or suggests they are evolutionarily related. Tawfik even says as much in the talk. Perhaps Brian Miller should have watched more of it?
But Brian Miller (or whoever wrote the quoted bit above) here talks about “functional proteins” being isolated points in sequence space. Not fold-based protein superfamilies. That is quite a conflation to make. The entire preceding discussion in Tawfik’s talk documents numerous cases of densely packed and different but overlapping functions within these structurally defined superfamilies(that within these superfamilies that conserve overall structure, one enzyme can be incrementally changed, while retaining structure and stability, to catalyze a radically, indeed fundamentally different chemical function). So “functional proteins” are by no means isolated.
Later in the talk, Tawfik goes on to explain that recent work has shown how there are examples known where these isolated structural superfamilies could have evolved from much shorter peptide sequences. So it isn’t necessary to postulate that any structurally defined superfamily ever changed incrementally into another by point mutations.
A single step would take on average less than 4N generations, where N is the effective population. but that doesn’t mean 1000 steps would take 4000N generations, since the second and subsequent steps could start spreading throughout the population before the first reached fixation. For sexual species, they wouldn’t even need to start in that subset of the population that already had the first step. So the best you could calculate would be a very pessimistic maximum.
For humans, assuming a generation time of 20y and a pre-agricultural effective population of 10,000 (which is what genetic studies suggest the population bottlenecked at 70kya) that would give a maximum time of 80 million years, and an expected time of maybe 10 million years.
But this is for humans. Modelling of eye evolution suggests that it might have taken about 2000 steps, partly successive and partly parallel, in creatures with shorter generation times, maybe 1 year instead of 20 years. That’d mean eyes would take less than a million years to evolve.
This doesn’t seem to be a problem.
 Wet finger estimate.
Obviously, you and @bjmiller will disagree A LOT about evidence and conclusions. I suspect that repeated sensible, evidence-based rebuttals (even if they actually are corrections) will not convince him otherwise. Miller may be engaging with arguments that are just plain wrong, but that doesn’t mean he is lying.
Well it’s difficult to see how it’s anything else when he’s been corrected twice on the same point. And that he’s now apparently repeated it a third time in another place.
Brian Miller can of course just come here and clarify how it is he keeps posting things that he’s been directly informed are wrong. He couldn’t find his glasses for 6 months straight? He just so happened to never read any responses when he posts here? Another case of Morton’s demon?
@bjmiller what’s your explanation?
It would be nice to be able to talk through the misconceptions, but the ID crew, for the most part, doesn’t seem interested in serious dialogue regarding evidence. Still, I don’t think accusations of lying are going to help anything.
You are of course correct. I’ll reformulate my initial response.
and what if we are talking about specific mutations? say that we want to change an active site into a another similar active site. so say that we need about 3 new specific mutations in specific locations. in that case i think that it indeed will take a long time.
Then you’ve abandoned evolution and are invoking the sharpshooter fallacy.
You entirely missed the basic argument. I was not addressing what selection could accomplish with functional proteins. I was addressing how stability changed with accumulating random mutations. The fitness dropped according to the negative epistasis model. Using Tawfik’s equation with his parameters, only an exceedingly small percentage of sequences would be stable if 10% of the amino acids randomly changed. More generally, the average drop in stability for a wide variety of proteins is around 1 kcal/mol, and the typical stability is less than 15 kcal/mol. Therefore, on average 15 random amino acid changes would completely destabilize most proteins.
The issue is the difficulty of a search through sequence space entering a region with a significant density of functional sequences for a given protein. Selection is not relevant until a sequence becomes marginally functional. You should watch Tawfik’s lecture on the state of protein research:
He describes different protein superfamilies as separate galaxies, and he describes how enzymes can only evolve within the confines of the same structure and same basic architecture for the active site. Based in his comments, the evolution of the first member of a superfamily should involve a search coming from a region in sequence space of nonfunctional sequences.
I think you’re projecting and don’t have the slightest idea how proteins work. You’re missing the evidence.
That’s utter nonsense, as you apparently don’t realize that stability is not correlated with function.
What you wrote in Quillette:
He also referenced the careful experimental work by Douglas Axe who used a technique known as site-directed mutagenesis to assess the rarity of protein folds in sequence space while he was working at Cambridge University from 1990-2003.
…was utter nonsense. Axe didn’t do anything of the sort. He deliberately started with a thermally unstable (temperature-sensitive) mutant and changed many amino-acid residues at once. He also wasn’t careful at all, because he couldn’t be bothered to assay enzymatic activity, which for the enzyme he chose was trivially easy to do.
If Axe thought that this was generalizable, he would have done the same thing to many other proteins. The fact that he quit with one speaks volumes.
What Axe did says absolutely nothing about the rarity of function (which you are eliding), the relationship between stability and function (Axe didn’t even assay stability), or “the rarity of protein folds,” (as pretty much any random sequence folds). Folds are a structural classification, not a functional one.
This has nothing to do with interpretation. You’re grossly misrepresenting the evidence itself, Brian, beginning with the truly nonsensical idea that stability is correlated with function.
The fact that you don’t engage in real discussion here, while repeatedly making the same false claims, is suggestive.
For an example of looking at the relationship between mutations, stability, and function, here is an example in our paper, which unlike Axe’s, was actually done carefully and thoroughly:
Kindly look at Figure 2 and think about it in light of your false assumption about stability:
You’ll see that every one of these disease-causing mutations increases stability. Did Axe measure stability?
How do you reconcile this evidence with your assumption that more stability is better, Brian?
Let’s not even get to evidence and conclusions. Let’s start with his assumption–that stability is pretty much equal to function.
Do you believe that, Curtis? Where’s the evidence?