Biologist Douglas Axe on evolution’s ability to produce new functions
| October 16, 2012 | Posted by News under News |
17 Responses to Biologist Douglas Axe on evolution’s ability to produce new functions
Leave a Reply
You must be logged in to post a comment.
Interesting (reminds us that as proteins are the workhorses of the cell, that is where the thing has to create novel functions first), links and papers?
related footnotes on Dr. Axe’s work:
Not only are functional proteins found to be extremely rare, thus undermining Darwinian presuppositions, but, as Dr. Axe pointed out in the OP video, the transition of any existent functional protein to a protein of a different function, by unguided Darwinian processes, is found to be of extreme, prohibitive, difficulty as well.
There is also very good, indeed overwhelming, evidence as to why we should expect such severe constraint on the ability of proteins to mutate, step by step, amino acid by amino acid, from one function to another different function. Proteins are shown to be ‘context dependent’, meaning that the entirety of the amino acid sequence of a protein domain is involved in a specific function and is not built up gradually. The following notes flesh this ‘context dependent’ characteristic of proteins out:
As well, functional proteins have now been shown to have a ‘Cruise Control’ mechanism, along the entirety of a protein structure, which works to ‘self-correct’ the integrity of a entire protein structure from any random mutations imposed on it.
Cruise Control permeating the whole of the protein structure??? This is an absolutely fascinating discovery. The equations of calculus involved in achieving even a simple process control loop, such as a dynamic cruise control loop, are very complex. In fact it seems readily apparent to me that highly advanced mathematical information must somehow ‘transcendentally permeate’ along the entirety of a protein structure, in order to achieve such control of the overall protein structure. This fact gives us clear evidence that there is far more functional information permeating proteins than meets the eye than simple rarity of amino acid sequences reveals (Szostak). Moreover this ‘oneness’ of cruise control, within the protein structure, can only ‘rationally’ be achieved through quantum computation/entanglement principles, and is inexplicable to the reductive materialistic approach of neo-Darwinism! For a sample of the equations that must be dealt with, to ‘engineer’ even a simple process control loop like cruise control for a single protein, please see this following site:
It is in realizing the staggering level of engineering that must be dealt with, i.e. ‘intelligently designed’ beforehand, in order to achieve ‘cruise control’ for each individual protein, along the entirety of the protein structure, that it becomes apparent that Axe’s 1 in 10^77 estimate for rarity of finding specific functional proteins within ‘sequence space’ is, in all likelihood, far, far too generous. In fact the probabilities over various ‘specific’ configurations of amino acids within sequence space, which have been one of the primary arguments against neo-Darwinism thus far, simply do not even apply, at all, since the ’cause’ for the ‘non-local quantum information effect’ within proteins does not even reside within the material particles in the first place (i.e. falsification of local realism; (Einstein, Bohr, Bell, Wheeler, Aspect, Zeilinger).
The following footnotes are further corroborating evidence that ‘protein specific’ quantum information/entanglement resides along/within the entirety of a functional protein amino acid chain constraining the chain to a specific function:
As to the ‘minor’ problem of protein folding itself:
Networking a few hundred thousand computers together has reduced the time to a few weeks for simulating the folding of a single protein molecule:
Not only are amino acid sequences of proteins shown to be ‘context dependent’ on the specific function of the protein, but, it turns out, that the function of the protein itself, in many cases, is context dependent on the specific function of the cell that a protein may be residing in:
Supplemental notes:
Here are further notes that support the position that existing functional proteins are severely constrained in their ability to mutate step by step into new functions:
As well, the ‘errors/mutations’ that are found to occur in protein sequences are found to be ‘regulated errors’:
In fact there is little hope of a truly random (i.e. Darwinian) mutation making it through the gauntlet of the ribosome:
Creationist and evolutionary biologist Todd Wood recently blogged about a recent study in Nature suggesting that protein evolution is much easier than typically claimed around here:
Anyone want to tackle how we can “spin this to support ID claims” ?
Great! Axe is really doing a wonderful work, on the most important problem.
So, just for clarity, I would like to remind a few numbers:
a) Behe suggest, in TEOE, an empirically observed limit of about 2-3 mutations (let’s say 13 bits maximum) for “evolution in action”.
b) I have proposed, many times, to use, for any biological context, an upper threshold of about 35 mutations (150 bits) as a really gross higher threshold in assessing dFSCI for a protein, computed, as usual, giving all possible exaggerated concessions to the neo darwinian model. My purpose was to lower DEmbski’s UPB (500 bits), and to have a more realistic threshold for biological events. That would be the upper limit of any biological RV transition.
c) Axe, using a model that is certainly much more accurate than my gross approximations, and supported by his personal experimental research, is offering here a veri credible empirical limit for the same thing: 6 mutations (about 26 bits).
I do believe that he is very near to truth.
My value of 150 bits is certainly too high, but my only purpose in proposing it was only to have a really unquestionable higher limit to say that a protein exhibits dFSCI.
Behe’s limit is empirical, and probably very realistic, but it is true that, if we want to consider transitions that could have occurred in very big Time Spans, his empirical models are too limited. Nehe’s limit remains absolutely valid for shorter Time Spans, and/or less numerous populations, and/or lower reproduction rate (such as multicellular organisms, and specifically mammals).
Axe’s value is extremely credible: it is in accord with mathemathical models and with empirical observations. It is, as far as I can say, the best assessment of what pure RV can, or cannot, do in a maximal biologic context (maximum Time Span, bacterial populations).
It is interesting to observe that a 6 AAs limit for random transitions would still allow for all microevolutionary events known (which are usually of 1-2 mutations most), and for much more (all the possible evolutionary events of 3-6 AAs complexity). But, at the same time, it would probably cut out of darwinian range many possible “intermediate complexity” events, such as many transitions in the context of existing structures and protein domains, as documented in Axe’s paper:
http://bio-complexity.org/ojs/.....O-C.2010.4
The origin of basic protein domains, obviously, cannot even begin to be considered, with these numbers.
But we can put them into an objective nested hierarchy, and that proves common descent by unguided mutation and natural selection is a better explanations, a trillions and trillions of times better explanation than ID, because an intelligent designer could have done it trillions of trillions of ways different.
Does anyone know if they have published the mathematical model they used?
JoeCoder:
Even if we take the study at face value, no-one disputes the idea that if there are functional intermediates that are easily obtainable through very minor changes, then the fitness landscape might be traversible from a to b to c. The question is, how often is this really the case?
After decades of searching for these intermediates (whether at the macro organismal level, or at the micro protein level), it is pretty well understood that, as a general rule, functional oases are sparse indeed. So the fact that researchers have identified, after years of effort and lots of research, an occasional potential intermediate in one or two cases is not really much help for the evolutionary story. In fact, a good argument can be made that these occasional results are the exceptions that prove the rule.
Hi GPuccio and All,
It is nice to be back. Can I ask you some questions, if you don’t mind?
1. Did you write up as a single note here at UD any of your interesting detailed comments that you posted some months back when you discussed these issues from the probabilistic perspective with Elizabeth Liddle, if I remember rightly? If you did, where can I find it, please?
2. I posted some notes on my blog and elsewhere and got myself some pretty tough arguments thrown in my face
Because I am not a biologist, I would be extremely interested to know your opinion:
2.1. Are you aware of Shaposhnikov’s experiments on aphids? It is claimed in the Russian biological literature that Georgiy Shaposhnikov actually succeeded in getting reproductive isolation of populations of aphids in as short a period as just three months (half a dozen generations, if I am not mistaken). Is it true, is it credible? Trouble is he always had to waste his time trying to defend himself from his hardline Darwinist colleagues who accused him of being a Lamarkist. Anyhow, this work that he did in the 1950-s-60-s has actually been published. Evolutionists in Russia rumour that not long before he died he continued his experiments and allegedly crossed the border of the aphid genus. This however was not published, so one can only guess. Whatever mechanisms were involved, epigenetic or not, he spotted reproductive isolation (he did not get as far as proving the existence of numerous progeny, because it required him waiting for some more generations of aphids, which he did not or could not do). I don’t know whether anyone else could replicate his experiments, and I don’t expect many people in the West to be aware of his work. Anyway, the point is, mutation rates can be extremely high. It is argued that such an extremely high rate of speciation is due to the fact that the selective pressure was a result of just one factor, type of host plant, literally nothing else.
2.2. As another example, I saw in wikipedia (well, yes, this notorious wikipedia) a page with alleged experimental proofs of evolution (many of those are strawman). But there among other things they claim that some reptiles actually developed in a timespan of just under 40 years some new functionality, novel organs of the digestive system. Your opinion on this? Could that have been a result of some latent genes which were not expressed until such times as something triggered it? I know very little in this, I just doubt it could be possible for true novelty to emerge without intelligent guidance (as usual with ID).
3. What I can’t quite understand in the business of protein evolution is that I don’t see how the hardness of new functional domain emergence/generation can disprove evolution at higher levels, i.e. at the level of tissue or whole organs. As far as I know, humans and bacteria use mostly the same proteins (correct me if I am wrong). If that is the case, evolutionists can say, okay, we don’t know the mechanism of new domains emerging but higher up in the organisation everything is explainable from the evolutionist standpoint.
Many Thanks.
Correction to 2.1. I rather mean speciation rates, not mutation rates (if these experimental results are true).
Dr S, good to see you. The lizards developed a valve, which other closely related lizards have, strongly suggesting activation of a pre programmed adaptation not incremental from scratch evo. I think the jury is still out on just what happened, per what was briefly reported, I would love more detailed comment. Cf blind fish. KF
OT: Here is another classic example of the ‘fit, damn you, fit!’ method of science that Darwinists practice:
Related notes:
See publications at the Biologic Institute for Douglas D. Axe and Ann K. Gauger.
See also Peer-Reviewed & Peer-Edited Scientific Publications Supporting the Theory of Intelligent Design February 1, 2012
See also Douglas D. Axe, and Ann K. Gauger, at Google Scholar
I’m glad that this kind of research is being done. If we can gather more evidence in this area (especially along the lines of the kind of research Ralph Seelke has done and Behe’s first adaptive rule) and publicize it, then almost half our work in the biological arena is done.
I’ll have to take another look at Edge of Evolution along with the criticisms of it. While the book may not have been 100% spot on in some respects, I think the basic points he raised in many of his examples still stand.
And it certainly is easier to see how isolated fitness peaks are from each other to get an idea of where evolutionary limits are rather than taking a given feature and estimating it’s probability of being produced by evolutionary means based on traits of that feature alone.
The former is more convincing to someone who buys into the idea that there is “no goal” of producing any given feature – and thus chooses to use that to escape falsification.
Eugene S:
Nice to hear from you again!
1. No, I did not post the whole reasoning as a single note. But I have recently discussed it and summed it up with Zachriel here:
http://www.uncommondescent.com.....ent-436926
at post #498.
The original diascussion is here:
http://www.uncommondescent.com.....selection/
The long discussion with Lizzie starts more or less at post #62, but you could look mainly at the last posts, especially #216.
I am very interested in going on with this kind of analysis, if anyone is interested in offering input.
2.1:
Any change that happens in such a short time is almost certainly not due to RV. It can certainly be the result of active adaptational mechanisms.
I believe that, given the chrinological frame, nothing is known about the molecular basis of the changes you refer to.
My firm view is that credible causal inferences about biological information can be done only where enough is known of the molecular mechanisms.
That’s why I never engage in discussions about phenotypic changes whose molecular basis is not known. That is also the reason why darwinists only speak of phenotypic changes whose molecular basis is not known. That often creates problems of communication between me and them !
2.2:
Please, see previous point. You say:
Could that have been a result of some latent genes which were not expressed until such times as something triggered it?
Absolutely. RV + NS is not even an option, with these time spans.
3:
Indeed, it’s the other way round.
First of all, basic protein domain go on emerging throughout the whole span of natural history, even if it is true that many of them emerged in LUCA, and the the rate of emergence constantly decreases in time. But even at the mammal level new domains continue to emerge. Therefore, if protein domains are a sign of design, then design has been going on throughout natural history.
But the important point is: protein domains are the simplest level of functional organization.
The only reason why I always discuss them, is that we have enough understanding of their molecular basis, and of the genes that encode the information for the. Afetr all, protin coding genes are the only part of the genome that we understand quite extensively.
At higher levels of organization, design is even more obvious that in the “simple” protein domains, but the analysis is more difficult. I will make some examples:
a) Behe has clearly shown that, at the level of molecular machines, the problem arises of irreducible complexity. Most proteins do not act alone, but are integrated in complex molecular machines, each of which is made of many different proteins, each extremely complex, each perfectly integrated with the other complex proteins, amny of them exclusive of the specific molecular machine.
The bacterial flagellum is still an unsurmountable problem for darwinism. Don’t believe the ad hoc propaganda of darwinists on that point: they have nothing to explain it.
And we have hubdreds, thousands, of other copmplex molecular machines whose functionall complexity is huge.
I don’t discuss them usually because, again, I need to bring the discussion to dFSCI calculation, to be able to make absolutely incontrovertible points, and it is much easier to do that with single strings with single defined functions, like individual protein coding genes.
b) Cell differentiation iin multicellular beings: that happens thorugh an extremely complex network of transcription factor and other components, whose workings we are just starting to analyze. As a consequence of that, a single genome implements hundreds of different transciptomes and proteomes, for each cell type and cell state.
That is a complete mystery at present. We have no idea of the procedures by which that is implemented. We don’t know how they work, and, especially, we don’t known how and where they are written and stored.
Of one thing I am certain: those procedures are mmuch more complex than protein domains.
c) The complex organization of organs and systems. Just two examples: the mammalian immune system and human central nervous system. Do you really believe that the spacial and functional organization of those machines, by far more complex and more efficient of anything else we know, are really a result of a few bits changed in the genome? Don’t believe it for a moment! That’s just the last, extreme, desperate lie of a false theory that has been clouding human cognition for decades.
GPuccio, KF,
Many Thanks for your comprehensive answers. I would have suspected that was the case regarding the lizards Podarcis sicula.
GP, I got your point regarding phenotypic change. It would be really nice if you could come up with an original post here that one can easily refer to.
Yes, function and rules (as opposed to constraints) are signs of intelligence for sure even more so in biosystems.