Charles Darwin’s theory of evolution is scientifically unlikely. The idea that all of biology just happened to arise spontaneously over long time periods (yes, that is what the theory of evolution says) is not motivated by the scientific evidence. This can be seen at all levels of biology including, more prominently in recent years, at the molecular level. A good example of this is the scientific evidence on proteins, and what it says about evolution. Read more
3 Replies to “Protein Evolution: A Problem That Defies Description”
Dr. Hunter, your golf course analogy would be appropriate if the golf course was the size of over 1 million galaxies and you had only one hole in that golf course. Moreover the size of that one hole in your golf course would be the size of a single sub-atomic particle of a single atom in those +1 million galaxies of your golf course (and even that example may fall far short of illustrating just how bad the problem of protein evolution is):
The Law of Physicodynamic Insufficiency – Dr David L. Abel – November 2010
Excerpt: “If decision-node programming selections are made randomly or by law rather than with purposeful intent, no non-trivial (sophisticated) function will spontan…eously arise.”,,, After ten years of continual republication of the null hypothesis with appeals for falsification, no falsification has been provided. The time has come to extend this null hypothesis into a formal scientific prediction: “No non trivial algorithmic/computational utility will ever arise from chance and/or necessity alone.”
Dr. Hunter: trying to get a comment onto your blog has been one of the most frustrating online experiences I can recall. I’ve opened a WordPress account; I’ve opened a Google Account–and still there’s always a glitch. Heavens!
This was intended for you blogsite:
I’m not going to write much because of all of the problems I’ve had trying to post here.
C. Hunter, in his 1-4-11, 1:41 post, laid out the rather severe problem this work presents. The authors write: “The evolvability of arbitrary chosen
random sequence suggests that most positions at the bottom of the
fitness landscape have routes toward higher fitness.”
Here’s the problem (and that is why the authors, earlier in the paragraph say that theirs is a ‘remarkable finding’): ANY random sequence can begin the climb up Mt. Improbable.
But….but…..this ‘proves’ Dawkins correct!!! Not exactly. But what it does point to (‘prove’ is such a strong word) is that there are no early constraints on a random sequence. Think about this for a second. What Darwinists suppose is that there are hidden natural forces which exclude sequences from forming, and thus LIMITING sequence space. But this is exactly what “doesn’t” happen. IOW, the incredible improbabilities calculated for strings of nucleotide bases are, in fact, valid. So, at the ‘base’ of these landscapes, anything goes. But once the climb begins, and above a certain threshold (approx 55% of target function), huge libraries of functional sequences are needed to continue the journey.
Bottom line: at the bottom of the fitness landscapes one a.a. is as good as another. That is: NO specificity required. Once above 55% of native function, EXTREME specificity comes into play. This is right out of the ID playbook!
Another day, another study, another sad day for Darwinism!
I can’t get anything posted at Darwin’s God Blog: so here’s a response (my final one for obvious reasons)
I have a question for you: in what way, specifically, does recombination help in the journey to higher fitness?
The limitation of evolution by only point-mutations is that it tends to get stuck on local maxima. Recombination allows it to move off these maxima. We can show that evolutionary algorithms that include recombination perform quite differently than those that only include point-mutation.
Let me begin by noting that the whole topic of recombination comes up as the authors talk about stagnation due to mutation-selection-drift balance. Well, what does this ‘balance’ really mean? It means that most mutations are deleterious, and that the work of selection is to rid the organism of these deleterious mutations more than anything else. Meanwhile, both beneficial and deleterious mutations can become fixed through random drift. In the end, some balance is reached between harmful and beneficial mutations due to these various forces.
Recombination allows the separation of beneficial mutations from harmful mutations, giving “evolution” a better chance to reach a higher “fitness”. That is, a portion of an “allele” destined to be eliminated with subsequent deleterious mutations can be replaced with a more ‘fit’ portion.
My reason for asking the question is to point out a very real fact in this experiment: at about 40% fitness (which, per the authors, is really no more than a single substitution from the original sequence—provided by E. Coli and the “libraries” they developed using PCR methods) the ‘adaptive walk’ gets stalled. One way of looking at this is the following: take some sequence that potentially can develop function, mutate it once, and it goes from 0 to 40%; but mutate it a second time, and its function is just as likely to decrease slightly as it is to increase slightly; and, so, the ‘adaptive walk’ terminates/stagnates. All of this simply points out the extremely limited effects of so-called ‘adaptive walks’ (=evolution).
lino235: If this were true, then nature would need to apply some kind of constraint to the sequencing. Where is this evident in this paper?
The constraint, in terms of the fitness function, is uphill until it reaches a maximum.
But, per the authors, the constraint is, at a maximum, 3 substitutions out of a string of 140, with most, apparently, being only single substitutions! This isn’t much of a constraint, is it? The authors therefore note this:
“Thus, the primordial functional evolution of
proteins may have proceeded from a population with only a small
degree of sequence diversity.” Doesn’t this really mean that “evolution” must start very close to the “fittest” sequence? Isn’t this the reason for the required 10^70 libraries? That is, if you whip up enough random sequences, one of them is bound to be within two or three a.a.’s of the native protein. That’s how I interpret this paper. And that’s why Dr. Hunter remarked upon it.