That’s fascinating, Gil, because you seem to have forgotten that less than 4 months ago you paid homage to Doug Axe:
I’d say that they are not scholars and that they are irrational.
Axe’s extrapolation, predictably misrepresented as fact by Meyer and many other ID creationists, was:
“…this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10^77…”
in the abstract, and
“So, if set S is about one-thousandth the size of set H (as above), then the proportion of all sequences of large-domain length that perform the specified function by means of any tertiary fold (i.e. fall within the dark portion of F) is estimated to be in the range of one in 10^77 to one in 10^53.”
in the discussion.
Note that Axe’s colleagues AFAIK have never acknowledged the other bound Axe set and only cite 10^-77.
So my question to you is how you reconcile the table you presented with Axe’s extrapolation (derived from a single experiment that a graduate student could finish in two weeks). Keep in mind that the table only includes 10 chosen structures and that there are many, many more in biology.
I see no contradiction at all between Axe ´s work and Tian & Best’s analyses presented in table1, quite the contrary.
Using different methodologies, both studies converge toward the same conclusion, ie., protein folds are very rare in sequence space.
And when the same conclusion can be drawn from different methods, it increases the confidence we can have regarding that conclusion.
I have a hard time seeing that 10^-77 for any functional protein and 10^-13 for villin specifically are not contradictory. Do you not understand exponential notation? Do you really think that being off by a factor of far more than 10^64 is not a contradiction?
“Very rare” isn’t quantitative. Moreover, as @Rumraket explained to you, you are grossly misunderstanding the paper from which you extracted the table to use as ammunition. This is what happens when you go looking only for data that support the conclusion you wish to be true. Science is about looking for the data that have the potential to show that you are wrong, something you clearly are afraid to do.
So explain the differences between the numbers in that table and Axe’s numbers, Gil.
And when someone enthusiastically posts numbers, but then retreats to describing things subjectively when they are shown to be contradicting themselves, we can have confidence that said someone is not seeking the truth.
First of all, according to table 2, the ratio of the target space on the sequence space (what the authors called SC*) for Villin is not 10^-13 but 4,7x10^-33!
Secondly, you cannot compare SC* for Villin and SC* for the beta lactamase fold studied by Axe since they have very different lengths ( the length of the Villin fold is 35 whereas the length of the beta lactamase fold is 153. For folds having similar lengths than beta lactamase, you should look the data for the last 3 folds at the bottom of table 1, ie., the alpha LA fold (123 résidus), the IFABP fold (131 residus) and the OmpA fold (171 residus). If you had done this, you would have seen that the ratios of the target space on the sequence space for these 3 folds are much smaller than what Axe has calculated for the beta lactamase fold, which undoubtedly strengthens the case that Axe is making, ie., that protein folds are very rare in sequence space.
The quantitative data are in table 1. For folds of similar length than the beta lactamase fold, their rarity range from 10^-111 to 2,6x10^-126. I myself would say that they are very rare in sequence space. Wouldn’t you?
My mistake (maybe). Then you’re only off by a factor of more than 10^44!
You clearly don’t know what “fold” means, Gil. Folds are structures of proteins, not the proteins themselves.
The same fold in different proteins can have dramatically different lengths because these folds include unstructured loops that can vary dramatically in length.
No. You seem to have forgotten that Axe’s figure was for ALL proteins, extrapolated from a single, cherry-picked case.
No need. Axe’s claim was global and not limited to beta lactamase.
We aren’t talking about that. We are talking about his extrapolation of that calculation to all of biology, remember?
The case he is making is quantitative, not qualitative.
No, but then I understand what folds are (structures) and I understand that those folds were made more specific by selection, so I understand how you are grasping at straws.
I really don’t understand the obsession with folds over functions. What matters is functions, not how those functions are achieved in some specific fold.
What possible use is it to say that TEM-1 Beta-lactamase folds might be as rare as between 10^-77 to 10^-53, when you can screen a library of about 10^8 antibody mutants and find the function (beta-lactam hydrolases)?
If a bacterium encounters a novel antibiotic like some penicillin, what matters here is that resistance is achieved, not that it is achieved through the TEM-1 beta-lactamase fold. That means if resistance is achieved through the catalyzed breakdown of the antibiotic. So the real question, then, is what is the frequency of protein sequences that catalyze breakdown of penicillin(?), not what is the frequency of some specific fold.
The function is demonstrably much more prevalent than some specific fold, hence the fold is completely irrelevant. What matters is if there is some protein, or some putatively expressed open reading frame, encoded in the genome of the organism, that can perform that function at a level visible to selection?
Since bacteria seem to be consistently able to evolve resistance to any imaginable drug, that frequency must high enough for that to consistently occur. Saying something else is to stand in denial of observational reality.
Exactly. And, most likely, thousands of Gil’s ‘n’ Bill’s have paid good money for it.
Some of the more valuable insights I have gained from this group are into the mindset of the type of person who is convinced by ID Creationist propaganda, and how stubbornly they cling to their misunderstanding no matter how clear the explanations they have received. It really is quite a spectacle.
I do wonder if this is a deliberate scam, or whether there is a symbiotic interaction going on, where the adulation and money pouring in from the Gil’s ‘n’ Bill’s helps quiet the demons of doubt that must exist somewhere in the recesses of the brains of the Axe’s and Behe’s.
A scam predicts a failure to engage or a pretense of doing so followed by flouncing. Sincere belief predicts a willingness to engage. This would be a gradient, of course.
The scam I am suggesting is from the DI. I don’t mean to suggest I doubt the sincerity of any of the members here. I just think they may be victims of people who, at least in part, know what they are doing.
The fact that you see the « explanations » we have received as clear and convincing demonstrate that you don’t understand the issues debated. I guess what it means is that one can enjoy a spectacle even without grasping it😀
As for you, aren’t you subjected to the demons of doubt in the recesses of your brain regarding your faith in neo-Darwinism. For example, what about this marvelous molecular machine involved in the camouflage of certain squid?
We just went through the camouflage discussion in the recent thread…
where I left you with a question…
All camouflage revolves around either facilitating a meal or avoiding being another’s dinner. Sometimes the strategy is opposite to camouflage. Poisonous animals are often as conspicuous as possible to advertise, make no mistake, this would be your last meal. That avoidance being established, some animals which are not actually poisonous mimic the gaudy coloration of poisonous relatives, and so are left alone. All of this blending in and standing out is solely based on two brutal truths of nature. One, if you are eaten, you are digested and die. Two, if you do not eat, you starve and die.
So my question is, how can you appeal to direct divine purposeful design of appearance, particular to each species, when it serves no other purpose than enabling such a nasty existence?
…
For so much of the animal kingdom, nearly everything about them revolves around predation. Their camouflage and appearance, their vision, their dentation, their speed, their digestive tracts, it is all about eating or being eaten. And you are saying this is the best of all possible designs, essentially that a good and benevolent God was intimately involved in the intricate details of a colossal system of death without which most species would even be recognizable? So what about this marvelous molecular machine involved in the camouflage of certain squid?
No, but the bigger point is that this is an apples/oranges comparison. Some might have some emotional resistance to accepting the evolution can account for this. But that’s a very different thing from the hard, mathematical facts you are having to ignore in order to maintain your position.
What an odd statement. Scientific theories shouldn’t be believed on faith, but accepted (or rejected) tentatively with a degree of certainty in proportion to the strength of the evidence in support of, or against them.
Given how good the evidence for biological evolution(which is more than just “neo-Darwinism”) is, even in cases where I don’t know specifically how some adaptation has evolved, I will err on the side of nevertheless betting that it evolved. But then a closer analysis of that adaptation in more detail has at least the potential to overturn my bet on evolution.
It’s just that every time that has been done in the past, upon closer inspection, the evidence for evolution has been overwhelming every single time.
At some point, after having seen the same horse thousands of times win every race it’s ever been in, it becomes completely irrational to keep betting on other horses.
That has nothing to do with faith. It’s evidence. But your projection is telling.
Good example. The molecular motors I’ve spent my career studying are very important in it. Have YOU studied it in detail to see if it is consistent with your wishful thinking?
If you have so much faith in design, why won’t you discuss the blatant contradiction between your adoration for Doug Axe’s tiny amount of work and the paper you chose to cite without reading it?
If you have so much faith in design, where is your design explanation for the amount of MYH7 variation in humans?
Note that Gil is ignoring the math in the paper he chose to cite. That’s pretty hard to do…
Axe has written a whole book centered on this incredibly lame experiment.