First off I must apologize for doing another post on a subject that’s been done to death around here, but I’ve been meaning to make a post about this for a while but other stuff kept coming up. Anyway, things have quietened down at work where I now only have to maintain some cell cultures, so I have a bit of time duing the christmas holiday.
My post, which is a repost of something I also brought up in a thread on Larry Moran’s sandwalk blog, is about a chapter in Stephen Meyer’s book Darwin’s Doubt and what I can, if I’m being generous, only attribute to extremely shoddy scholarship.
Having read the book, a recurring phenomenon is that Meyer time and again makes claims without providing any references for them. Take for instance the claim that the Cambrian explosion requires lots of new protein folds, from Chapter 10 The Origin of Genes and Proteins:
“Axe had a key insight that animated the development of his experimental program. He wanted to focus on the problem of the origin of new protein folds and the genetic information necessary to produce them as a critical test of the neo-Darwinian mechanism. Proteins comprise at least three distinct levels of structure:4 primary, secondary, and tertiary, the latter corresponding to a protein fold. The specific sequence of amino acids in a protein or polypeptide chain make up its primary structure. The recurring structural motifs such as alpha helices and beta strands that arise from specific sequences of amino acids constitute its secondary structure. The larger folds or “domains” that form from these secondary structures are called tertiary structures (see Fig. 10.2).
Axe knew that as new life-forms arose during the history of life—in events such as the Cambrian explosion—many new proteins must also have arisen. New animals typically have new organs and cell types, and new cell types often call for new proteins to service them. In some cases new proteins, while functionally new, would perform their different functions with essentially the same fold or tertiary structure as earlier proteins. But more often, proteins capable of performing new functions require new folds to perform these functions. That means that explosions of new life-forms must have involved bursts of new protein folds as well.”
In the whole section Meyer dedicates to the origin of novel folds, he makes zero references that actually substantiates that the cambrian diversification, or indeed any kind of speciation, or the that new cells types or organs, requires new protein folds. ZERO. Not one single reference that supports these claims. At first It reads like what I quote above, lots of claims, no references. Later on he eventually cites the work of Douglas Axe that attepts to address how hard it is to evolve new folds(and that work has it’s own set of problems, but never mind that). Axe makes the same claim in his ID-journal Bio-complexity papers (which eventually Meyers cites), but in Axe’s papers, that claim is not supported by any reference either. It’s simply asserted as fact. In other words, Meyer makes a claim, then cites Axe making the same claim. Neither of them give a reference.
Meyer mentions Ohno:
“The late geneticist and evolutionary biologist Susumu Ohno noted that Cambrian animals required complex new proteins such as, for example, lysyl oxidase in order to support their stout body structures. When these molecules originated in Cambrian animals, they also likely represented a completely novel folded structure unlike anything present in Precambrian forms of life such as sponges or one-celled organisms. Thus, Axe was convinced that explaining the kind of innovation that occurred during the Cambrian explosion and many other events in the history of life required a mechanism that could produce, at least, distinctly new protein folds.”
No reference is given here either. The claim is simply made initially, so it’s hard to check. Is Meyer and Axe willing to bet that a preceding evolutionary history of, for example, Lysyl oxidase cannot be found in structure and sequence of related molecules? That there ARE no related molecules? Is that his claim? That the Cambrian explosion required tonnes of bona fide Orphan proteins with no preceding history? Where are the references that support this? Did Meyer or Axe look for homologues of Lysyl Oxidase and found none?
It gets much worse, turns out Meyer is making assertions diametrically opposite to what his very very few references say. Remember what Meyer wrote above?
“The late geneticist and evolutionary biologist Susumu Ohno noted that Cambrian animals required complex new proteins such as, for example, lysyl oxidase in order to support their stout body structures.”
Well, much later in the same chapter, Meyer finally references Ohno:
“Third, building new animal forms requires generating far more than just one protein of modest length. New Cambrian animals would have required proteins much longer than 150 amino acids to perform necessary, specialized functions.21”
What is reference 21? It’s “21. Ohno, “The Notion of the Cambrian Pananimalia Genome.”
What does that reference say? Let’s look:
“Reasons for Invoking the Presence of the Cambrian Pananimalia Genome.
Assuming the spontaneous mutation rate to be generous 10^-9 per base pair per year and also assuming no negative interference by natural selection, it still takes 10 million years to undergo 1% change in DNA base sequences. It follows that 6-10 million years in the evolutionary time scale is but a blink of an eye. The Cambrian explosion denoting the almost simultaneous emergence of nearly all the extant phyla of the kingdom Animalia within the time span of 6-10 million years can’t possibly be explained by mutational divergence of individual gene functions. Rather, it is more likely that all the animals involved in the Cambrian explosion were endowed with nearly the identical genome, with enormous morphological diversities displayed by multitudes of animal phyla being due to differential usages of the identical set of genes. This is the very reason for my proposal of the Cambrian pananimalia genome. This genome must have necessarily been related to those of Ediacarian predecessors, representing the phyla Porifera and Coelenterata, and possibly Annelida. Being related to the genome – possessed by the first set of multicellular organisms to emerge on this earth, it had to be rather modest in size. It should be recalled that the genome of modern day tunicates, representing subphylum Urochordata, is made of 1.8 x 10^8 DNA base pairs, which amounts to only 6% of the
mammalian genome (9). The following are the more pertinent of the genes that were certain to have been included in the Cambrian pananimalia genome.”
The bold is my emphasis. I trust you can see the problem here. So, Meyer makes a single goddamn reference to support the claim that the Cambrian explosion required a lot of innovation of new proteins, folds, cell-types and so on. What do we find in that references? That Ohno is suggesting the direct opposite, that he is in fact supporting the standard evo-devo view that few regulatory changes were what happened, that the genes and proteins were already present and had long preceding evolutionary histories.
Later Meyer gets a ID-complexitygasm when he asserts, again without any support, that:
“The Cambrian animals exhibit structures that would have required many new types of cells, each requiring many novel proteins to perform their specialized functions. But new cell types require not just one or two new proteins, but coordinated systems of proteins to perform their distinctive cellular functions.”
Where does he get this? His ass, that’s where.
Rumraket,
Sorry for the misreading.
I’m not wrong about any of this. You are welcome to re-read the op over and over again until it sinks in. Meyer is arguing that lots and lots of new protein folds had to arrive de novo in the cambrian explosion. Not before, not after. In the cambrian explosion. And because, clearly, there is not enough time in the cambrian explosion for all that de novo protein fold invention, then something else than evolution must be responsible. That’s the whole idea.
That’s also what you yourself understood about it, to begin with, before you realized how clusterfucked Meyer really is, when you stated multiple times you intuitively agreed with Meyer. It made sense to you that new animals forms arising in the cambrian would require new protein folds. It made sense to everybody. It made sense to me (it’s the kind of thing that superficially makes sense, before one learns about evo-devo). It made sense to all the ID-friendly reviewers of this book, writing blurps on his website.
But now and suddenly some curious phenomenon is at work. It seems you’ve forgotten all about what you initially understood Meyer to be arguing.
Scurrolous. 🙂
I find that funny, because another favorite of IDists, Koonin, wrote a whole book about the evolution of proteins and never mentioned any discontinuities.
The only way you find discontinuities is to ignore biology. Even Behe doesn’t do that.
Has Behe reviewed Darwin’s Doubt?
I haven’t found it on google.
http://darwinsdoubtreviews.blogspot.com/2013/09/charles-r-marshall-reviews-darwins.html
If anyone doubts that Meyer is a fundamentally dishonest person.
This is Meyer’s cdesignproponentsist.
No it does not. Same function doesn’t imply same structure especially since the residues are different. This means it achieves similar function DESPITE different structure. The paper details the various loops and chains missing or inserted vs. other LOX implementations, which means they are folded differently.
You misinterpret the article, and to disabuse you of the notion that same function implies same structure, I refer you to evolutionary literature:
The paper points out there are some enzymes with no homology and other with only active site “homology” (convergent similarity) but are otherwise different outside the active site. These citations shatter your implied claim that similar function implies similar molecular structure. Not so. Meyer is right, the OP fails.
This also has a bearing on what you said.
Statements like that indicate the OP is failing. High similarity indicates common descent. Now you say low similarity also indicates common descent. Hence nothing in principle can falsify common descent, which suggest the claim of common descent is fundamentally a faith axiom, not a falsifiable claim.
Fer all ya know, it might have been providential evolutionary convergence or (gasp) special creation.
You see that phrase “convergent evolution”? That’s a euphemism for similarity that is not due to common descent.
I avoid that problem by always viewing my own words in color.
That’s my specialty! That and complaining about moderation.
I didn’t say the same function implied the same structure. Sal, you’re simply not reading what I write. I’m not elucidating that because it has a similar function, it must (or is suggested to) have a similar structure. I’m reading what it says right there in the abstract. That it is similar in structure AND function. It is an observation, not an implication.
No, the residues being different does not mean it has a different structure. After all, that is what it means to say that the structure can be conserved despite the sequence being different.
Yeah, while it is still clearly structurally related to other lysyl oxidase, it nevertheless also has changes.
A notion I have not suggested, or believed, or even implied.
In fact I’m well aware of the fact that there are known cases of totally dissimilar structures being able to perform the same functions. This is one of the reasons why similarity in structure implies common descent, but mere similarity in function does not.
For example, birds and bat wings are similar in function, but not in structure. They do not derive from a common ancestral wing, just because both function as wings.
So you have access to the paper now? I can’t comment on it’s contents beyond the abstract until I get to work tomorrow.
Since this was never implied, there is nothing to shatter.
Not so. Meyer is wrong, your reading comprehension is what have failed. It’s starting to look like you’ve borrowed Mung’s Demon.
You seem to think that because I wrote two statements, one after another, separated by a period, that means the first sentence implied what I wrote in the second one. Not so. Rather, I was merely re-stating what it said right there in the abstract. That it is BOTH functionally AND structurally related. I have not implied anywhere, nor believed even for a second, that just because one enzyme can do the same job the other can, that means the structure must be similar.
No my friend, I merely read the abstract. You know, where it says:
Similarity in either sequence, or similarity in structure and function, yes.
No, I don’t. Anywhere at all. The fact that there is conservation of both structure and function is what implies common decent. The sequence dissimilarity obviously does not. Nor have I implied that it did. Again you seem to have taken the fact that one part of a sence sentence was written after another, as insinuating the first part of the sentence implied the second one. Which is strange, because the word “but” was after the comma.
Here’s a hint: When I mean to imply something, I usually write “this implies”, or “which supports”, or “therefore…”.
But what I actually wrote was: ” The sequence changes over time, but the overall structure and function is more conserved over time.”
Notice the ‘but’, which I have now bolded. This implies (heh) that the implication of the first part of the sentence (that there is no common decent because low sequence similarity) was overruled by the second part (but there IS common decent, because there is high structural AND functional similarity).
Sal, stop flailing and read what I write.
It’s as if stcordova hasn’t had any training at all in biochemistry or molecular biology.
On the contrary, I have been remarkably consistent.
This is from my first post in the thread:
Now does anyone actually believe that all that proteins present in all the Cambrian animals already existed in some common ancestor?
And from my second post:
I’ve been on the same course throughout.
In the actual argument made by Meyer quoted in your OP, which I quoted in full HERE, I do not see any lies.
I was attempting to walk through it, statement by statement, to discover which statements were false. No one seems interested in following along though. Odd that.
Perhaps, like Elizabeth, people just “know” that Meyer is a liar. Must be somewhere else though, somewhere other than in the quoted text
Yeah, as in different folds since it has different chains!
My Demon is hard at work.
So feel free to explain to the readers how missing chains and inserted chains imply the folds are identical. Seems to me if that’s the case, they have to fold differently as a matter of principle. We’re not just talking point or amino acid residue mutations.
To complain Meyer could have improved his case with citations, Ok. To complain Meyer is wrong that there aren’t novel folds, nope. The data indicate the folds are novel.
Whether they are needed is a separate question, but if you want to insist to all the readers out there that missing and inserted chains imply the same folds, go right on ahead, but I couldn’t live with myself making such dubious assertions.
Maybe the moral of the story is don’t beat on a dead horse.
We seem to be losing the thrust of Meyer’s thesis. His thesis seems straightforward:
1) The Cambrian was a relatively brief period of wildly proliferating body plans.
2) These different plans imply different protein folds.
3) A great many new body plans implies a great many new folds.
4) New folds cannot naturally evolve at this speed.
5) Therefore an intelligent designer is required.
This sequence makes much more sense to me, and perhaps others here, if it is somewhat inverted.
1) GIVEN that an intelligent designer exists, how can we show it?
2) GIVEN that life is so enormously complex in every detail, it could not have happened naturally.
3) Here is a period when alleged “natural” processes could not have kept up, specifically with new protein folds.
4) THEREFORE, goddidit, which we knew as a given anyway.
This reflects the difference between the scientist (“here are the facts, what conclusions can we draw from them?”) and the creationist (“here are the conclusions, what facts can we misrepresent to support them?”)
Whichever sequence seems more reasonable, the objections are the same: that in fact very few new protein folds occurred during this period, that in fact nearly every protein used in these constructions existed before the Cambrian, and that in fact these facts were (or should have been) well established and known to Meyer before he wrote the book.
The best-fit explanation is that Darwin’s Doubt is apologetics and not science.
Ok,
There are graphics of the yeast PPLO folds done by crystallography, this one supposedly can be viewed like a hologram if one had stereoscopic viewers:
http://journals.iucr.org/d/issues/2006/09/00/wd5066/wd5066fig1.html
There are no images of the mammal lysyl oxidase for whatever reason. The literature acknowledges the structure mammalian lysyl oxidase has not been elucidated!
We could settle the novel folding debate rather easily if we had some graphics.
In lieu of graphics, I refer the reader to the UniProt databse for the one hit of lysyl oxidase that also had Anthony Duff mentioned in the notes. It lists it under Amine Oxidase, but it clearly references Duff’s paper which I mentioned. There 787 residues for the yeast PPLO:
http://www.uniprot.org/uniprot/Q96X16
compare this to human LOX1 which has only 574 residues:
http://www.uniprot.org/uniprot/Q08397
The way the copper is connected to the proteins is different in yeast vs. mammals which implies the physical connection geometry must be different as a matter of principle (different fold!).
The Human has a lysine tyrosylquinone cross-link (LTQ), the yeast does not.
I read that to mean the Human LOX uses an active site helper molecule (LTQ), an active site co-factor which the yeast does not. They are structurally different, they are folded different.
All that has been put forward by the opposing comments is that they have the same fold, with NO DATA. I’ve provided data above.
My opponents in this discussion insists the yeast and mammalians have identical folds. At best it is unknown, at worst it is false. Thus, the OP then cannot unequivocally declare Meyer wrong on the issue lysyl oxidase.
Wikipedia contrasts TPQ (in yeast) vs LTQ (in humans):
https://en.wikipedia.org/wiki/Lysyl_oxidase
The cross link in humans is residues 477-512, and totally non-existent in the yeast. How can this be consistent with them folding the same identical way? If the OP wants to insist that, fine, I would not want to be telling science students they have identical folds in the absence of data and in the presence of data strongly suggesting otherwise.
The data at worst don’t refute Meyer, and may actually support his (and really Ohno’s claim) regarding the change in structure of lysyl oxidase.
Folding, shmolding. Nice job of deflecting.
Once again: It’s the phylogeny that counts.
Deal with it.
Red herring: Folds don’t have to be identical.
Seems to you. That’s a great argument.
What principle?
I provided the protein sequences above, you construct a phylogeny. 🙂
About all you have is the methionine residue “M” to start each one, but that doesn’t mean much because virtually all proteins start with M!
The reader can see for themselves given the sequences how dissimilar they are, exactly as characterized by the quotation I provided:
Let the reader look at the sequences! Looks like your phylogeny hit a dead end. 🙂
stcordova,
Well, I think phylogeny is fundamentally what matters here. If there is continuity of function, and continuity of descent, I don’t see how we can have a robust conclusion that animals invented a new protein to perform the lysyl oxidase function.
“We identified LOX proteins not only in animals, but also in many other eukaryotes, as well as in bacteria and archaea – which reveals a pre-metazoan origin for this gene family.”
Here’s the Nature paper, painfully focused though it may be.
Certainly looks like there has been gene duplication and specialisation for different tasks in multicellular vs ancestral forms. But I don’t see any of these fit the bill as a ‘new protein’ in the way I would understand that admittedly hazy term.
[eta: ninja’d by Pedant!]
It’s been done. Don’t you read the previous posts in a thread?
http://www.nature.com/articles/srep10568
You’ve contributed nothing but noise to the argument.
Mung,
I did? Two hurried one-liners prompted directly by something you said is a tangent, now? I actually went off to see Star Wars with the kids.
See! I knew you went off on a tangent!
😉
I hope they enjoyed it. How long till you go see it again? 🙂
There are only about 1300 different folds in the entirety of the proteins in all species examined. There are clearly not just 1300 different amino acid sequences. So something about Sal’s assumptions must be off. The same fold (as classified) can clearly be achieved by many amino acid sequences, given 10-20,000 proteins per organism and God-knows-how-many genomes sequenced.
A fold does not need to be ‘identical’ to another to be, to all intents and purposes, the same fold. People seem stuck in a digital view of amino acid space, where substitution of one acid by another leads to a radically different result. It doesn’t, if the new acid maintains chemical property. You can replace the entire amino acid sequence, one by one, and still retain ‘the same fold’ at all points of the process. You end up with no sequence homology.
Mung,
Once is fine! But the green planet‘s just up the road from me.
Let’s look at what he actually wrote:
New animals typically have new organs and cell types, and new cell types often call for new proteins to service them.
New animals typically have new organs and cell types, and new cell types often call for new proteins to service them. In some cases new proteins, while functionally new, would perform their different functions with essentially the same fold or tertiary structure as earlier proteins. But more often, proteins capable of performing new functions require new folds to perform these functions. That means that explosions of new life-forms must have involved bursts of new protein folds as well.
Hey Allan, could you say something about the relationship between protein folds and domains? Any relationship worth talking about? Thanks.
But, but, but, but….
What about the isolated islands of function?
Mung,
The distinction is a little bit hazy and interchangeable, but domains tend to be functional units and folds structural. They occupy a similar level in the hierarchy of protein structure, between secondary and tertiary.
Sequence is primary structure, and this often folds into secondary structures – alpha helixes, beta sheets – which arrange at a higher level into domains/folds, one or more of which becomes the tertiary structure of a complete protein.
There is some unavoidable cross-talk between the effect of a region on folding and its effect on function. There are obviously two primary things a protein has to do: fold correctly and then work. Parts of the structure that are involved in folding do not necessarily have any role in the finished product. Separate folds enable a protein to fold faster – each ‘fold’ within the larger protein is separately folding at the same time. But separate domains (while being unavoidably involved in folding) allow multiple functions to be performed by the one protein, eg DNA binding and cleavage might be performed by separate domains of the same protein.
I just finished re-reading Chapter 10 of Darwin’s Doubt. First, the phrase “body plan” doesn’t even appear in the chapter. So if we want to discuss Chapter 10 let’s discuss what it’s actually about. Fair enough?
Maybe I’m not reading this thread competently. What I’ve been given to understand is that this intuition turns out not to be the case — that is, the “new organs and cell types” did NOT result from a burst of new protein folds. The analogy I envision is the intuition that a burst of new photographic subjects “must involve” a burst of new photographic technologies. But instead, the new organs and cell types were mostly (not entirely, but mostly) the result of changes in regulatory functions, not changes in proteins.
I’m certainly no biologist, but I suspect claims that new cell types “often call for” new proteins. I have no difficulty imagining plenty of cell types constructed from the same ingredients. You would be amazed what I can do with nothing more than flour, sugar, butter and eggs.
In any case, Meyer is not deriving his Designer from his assumptions, he is constructing his assumptions so as to “find” the Designer he knew was there all along. Even if this means misrepresenting or ignoring ALL the literature on the subject available to him. Which is the hallmark of doctrinaire creationism.
I think that Rumraket has already done this, but here’s my independent re-work of the offending paragraph:
New animals
typicallyoccasionally have new organs and cell types, and new cell typesoftensometimes call for new proteins to service them. Insomemost cases new proteins, while functionally new,wouldperform their different functions with essentially the same fold or tertiary structure as earlier proteins. Butmore oftenoccasionally, proteins capable of performing new functionsrequiremake use of new folds to perform these functions. That means that explosions of new life-formsmustneed not have involved bursts of new protein folds as well.Having just re-read Chapter 10 of Darwin’s Doubt I have to say that other than quoting from the same chapter the OP has little resemblance to the actual content of the chapter.
The chapter is about Douglas Axe’s work with protein folds and has little to nothing to do with the Cambrian explosion itself other than to conclude at the end of the chapter that given everything in the preceding pages of the chapter that “neo-Darwinism does not explain the Cambrian information explosion.”
On numerous occasions in the chapter it plainly states that the numbers used are based on the entire history of life, and not just the period prior to and including the Cambrian.
Once again we find an OP against Meyer’s Darwin’s Doubt that is nothing more than a straw-man. More like beating a live horse and then shooting and then claiming you were beating a dead horse. In a way, you were.
Gawd, I just made an argument worthy of Elizabeth herself.
I’d appreciate you don’t attribute assumption to me that I don’t profess. I never said nor insinuated the number of folds discovered in biology is as immense as amino acid sequence space. Denton pointed that out in a peer-reviewed paper:
http://www.ncbi.nlm.nih.gov/pubmed/12419661
So your response is based on something that is not true, and I accepted Denton’s small number of folds long before you just attributed an argument to me which I did not make…
Regarding Meyer’s words, was he saying a “new class of protein folds” or “existing protein sequences being subject to new folds with minor sequence change”. One can object to the wording, I have no issue with that. Meyer could have said “acquiring a fold it didn’t have” and that would have settled the ambiguity.
What I did have issue with is the assertion of the lysyl oxidase protein in yeast as somehow refuting Meyer’s assertion. The sequences are there above for all to see and they have no sequence “homology” worth speaking of.
Additionally, the listed post translational modifications and the sheer size difference suggest different structure.
Notice the localities of the disulfide bonds which affect folding:
for Yeast:
for humans Lox1:
They could easily be folded differently.
If one interprets Meyer words differently, then he is perfectly consistent with papers such as this:
The author points something out that gave me a chuckle
Universal Common Ancestry (UCA) is found to be almost useless yet again. Similarity proves similarity, no need for UCA to see it, in fact UCA clouds taxonomical conceptualizations.
One thing to note:
I find this confusing. FIRST you say that Axe’s work has “little or nothing to do with the Cambrian”. THEN you say that this chapter “concludes” that “given what was in the chapter” the Cambrian is not explained. THEN you say, again, that you’re talking about the entire history of life, not just the Cambrian!! But if the chapter was not about the Cambrian, and was in fact about the entire history of life, HOW do you draw conclusions about the Cambrian from material you yourself say (twice) does not address the Cambrian?
One might also wonder why a chapter of a book specifically arguing that the Cambrian refutes Darwinian processes, has a chapter irrelevant to the Cambrian, which nonetheless draws conclusions about the Cambrian.
stcordova,
And nor is that what I was saying. Your ‘assumption’ I referred to was that the yeast and mammal LOX genes should be regarded as unrelated due to lack of sequence similarity. (Even this is over-egged: they do not lack sequence similarity; it is low. But it is there. Similarities down to 30% – only 5% above completely random alignments of a 4-base code – are regarded as significant).
But since, in my point, the same fold can be supported by many different amino acid sequences – including, very often, a path that involves stepwise substitution of the entire primary sequence – then one has to include that possibility in one’s assessment. The Nature paper does not support a conclusion that the Yeast and mammal LOX genes had an independent origin.
The thing about reconstructing phylogenies is that you don’t generally just have 2 sequences. So while you might, if you only had 2, be able to support your contention that “Universal Common Ancestry (UCA) is found to be almost useless yet again. Similarity proves similarity, no need for UCA to see it, in fact UCA clouds taxonomical conceptualizations.”, if you have a rich enough dataset you can see the intermediate pattern more clearly. A favourite analogy is with language. The number ‘eight’ is variously rendered acht, ashta, huit, otto, octo, ocho, wyth, eight, etc among Indo-European languages. Some have one syllable, some 2; the typical pattern is a vowel, a hard sound and possibly another vowel sound. If you only had ocho and eight, you might get away with ‘similarity proves similarity’ (and they aren’t all that similar). But with a wider dataset, that line begins to look more and more like deliberate blindness to the pattern. Your position on phylogeny appears to be (though you may not realise it) that we are hamstrung by almost always only being in possession of 2 members of a dataset, and 2 character states to compare.
Beyond that I do find it amusing that a YEC – who presumably thinks the base of the Cambrian is the bottom of Flood deposits – is supporting Meyer, who clearly doesn’t. And you are trying to dismember phylogeny, on which, rather shakily, Meyer’s argument rests. He accepts phylogeny in principle, but tries to argue that ‘many folds’ do not relate to sister groups at this Cambrian boundary. He’s not saying universal phylogeny is bunk (he may think it, but he isn’t really entitled to any conclusions from it if he does).
It seems to me that the important point is this: Meyer cites Ohno to support a claim directly opposed to what Ohno said.
It seems to me important that Ohno is not tho only person quotemined, or even the worst case. Other quotes are fabricated. Assembled from two quotes with no indication they are from separate sections.
It also seem significant that whenever such bad quotes appear, they support a conclusion opposite of the one intended by the original author.
If we’re discussing chapter 10 of Darwin’s Doubt, it’s all about folding.
Please open your copy of the book to Chapter 10 and read it.
Thank you
Meyer, iirc, argues that this makes them very rare in sequence space. I’m sure you would disagree with that though.
Is there any fairly easy way to ascertain how many different sequences lead to these same folds?
That’s a valid question, asking how Meyer reaches his conclusion. But until people are wiling to address the actual argument I don’t much see the point of getting into it just yet other than to say what I have already said, which is that his premises are different from his conclusion.
And none of this makes him a liar.
I intend to create a follow-up post on the extent to which Meyer actually references the Cambrian during the course of the chapter.
By the way, it’s chapter 13 that is on the origin of body plans, not chapter 10. The OP is about chapter 10.
I still see signs in this thread that people think Meyer is a young earth creationist.
🙁
Meyer argues, in chapter 10, that the work done by Douglas Axe demonstrates otherwise. Has Axe’s work been refuted?
Mung,
Yes.
But this is an unwarranted conclusion. If one regards evolutionary processes as the motor for providing new functional proteins, then those processes start with small changes to existing sequences (even duplication adds a second copy of an existing sequence). So evolution does not need to search all sequence space to find new functional proteins, there seems to be rich functionality in the local space. So there’s no reason to think that total sequence space is not also rich in unexplored functionality. And experimental data so far supports the idea that potentially useful sequences can be found. Keefe and Szostak being the classic example.
As always thank you for reading and responding. Even though we’re usually in sharp disagreement, I often come away from the discussion with something of value personally. If nothing else, make me want to keep studying chemistry.
With respect to your claim, because of the limited number of folds in living organisms, it is true there will be structural correlation with as little as 12% pairwise identity.
http://peds.oxfordjournals.org/content/12/2/85.full
Sure, if you have an alpha helix in one protein, why shouldn’t we expect an alpha helix in some other protein somewhere since alpha helices are ubiquitous. But the overall protein could be different. And alpha helices abound and so do the tertiary structures they result in.
FWIW, I ran blast on the sequences, and I got the following results:
http://blast.ncbi.nlm.nih.gov/Blast.cgi
Query cover 25%
Identity 34%
I take that to mean 25% was even able to be aligned and that means 75% was not, and of the 25% that was aligned, it only had 34% identity.
25% of 34% = 9%
So there is some parts we can align, but that doesn’t look that much above random. Convergence could just as well be argued!
I realized when I looked at the list disulfide bonds plus the other Post Translational Modification (PTM) such as the LTQ and TPQ, they are highly residue specific. The Lysyl Oxidase will fail without those Post Translational modifications. It is perfectly reasonable there is some tolerance for change, but there is an amount of change that will cause a breakdown in the existing PTM machinery. At some point enough DNA changes to the LOX gene will require corresponding PTM changes, and no really knows where the blue prints and instructions for the PTMs are, much less do we know how they can be successfully modified. For example, the Yeast had the following disulfide bond:
The Human had the following PTMs:
Imho, these can’t change willy nilly. Sure we might mutate that DNA till the coded sequence is unrecognizable, but we can’t just assume the protein will have reasonable function without corresponding changes in the PTMs.
If Meyer had not used the word “folds” but rather “post translational refinements that include changes in folds, chemical cofactors, glycan association,…..” that may have been a better framing of issues of transforming existing proteins to new function with minimal sequence change. In the case of Lysyl Oxidase, the changes were substantial. The glycolization PTM changes may also be significant considering more than half of the cellular information processing is in the glycome (according to the NIH glycome website).
As far as the benefit of assuming phylogeny, I don’t see it, it’s superfluous, what really counts is similarity and non-similarity. Richard Owen before Darwin defined homology in terms of similarity and carried out comparative anatomy without the assumption of common descent. There are just floods of papers that speculate on phylogenies that cannot be resolved any way, and which give next to no operational insight that couldn’t be gleaned by just going about business the way Owen did.
Patrick, are you saying that Axe’s peer-reviewed published work was refuted in a blog post?
I don’t like it when people quote-mine me.
Talk about beating a dead horse- there still isn’t any evidence that natural selection, drift and neutral changes can produce/ produced the diversity of life. We have no idea if changes to genomes and the way they are regulated can produce the changes necessary. And we can’t even test the claim.
So perhaps that is where you guys should focus.