You are claiming they explore them in the same way and your prior description does not support this.
Not sure what you mean: in evolution, proteins evolve through random mutations and subsequent selection. For antibodies, it’s the same: random mutation, followed by selection.
Yes I would like to understand this better. Regarding the Behe claim if you assume the genome size he was quoting from is the same you are quoting from then I stipulate that his edge was a little too tight 
The problem with Behe’s argument is that he determines his “edge” based on multiple simultaneous mutation events. The problem for Behe is that evolution works just fine through sequential (i.e. one after the other) mutation events. Behe’s entire argument fails because it ignores how evolution actually works.
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Hi Dennis
What I have read so far does not support this claim. This may be my education level but it looks like the upfront process is not a completely random search of all the amino acids available.
Lets agree to disagree at this point but I stipulate this may be my current understanding. I will do further reading. Any references you can provide would be appreciated.
I think that this is a valid criticism that Mike’s hypothesis is not universal to all evolutionary scenario’s. I have a lot of respect for Mike and believe that he would be open to a solid counter argument.
Hi Bill,
The binding specificity of a particular antibody is determined by about 5 - 10 (or so) amino acids in the variable domain region. One antibody is formed from two such variable regions, that are independent from each other. That said, all amino acids in the variable domain can be mutated, and all possible amino acid substitutions are seen (since the process is randomized through somatic hypermutation even beyond what is accomplished through V(D)J recombination).
Here’s a portion of a textbook discussing this:
Thanks Dennis 
Hi Eddie -
Thanks - just keep in mind it was a comment,on a blog post, summarizing a large body of experimental evidence. I feel that this conclusion (that RAG 1 and RAG 2 are exapted transposases) is as solid as human/chimp common ancestry. So, in a brief comment, I was fine with using the indicative. I might do a series on the evolution of the vertebrate immune system at some point, where I will lay out the evidence behind that brief gloss.
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[quote=“Billcole, post:109, topic:9418”]
What I have read so far does not support this claim. [/quote]
Are you reading any biology?
[quote]This may be my education level but it looks like the upfront process is not a completely random search of all the amino acids available.
[/quote]Neither one is. That’s why they are the same!
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Here’s an excellent section from that review:
The silliest argument against natural selection
But without a doubt, Axe’s silliest argument against natural selection is that it cannot invent. He calls this the Gaping Hole in Evolutionary Theory (p. 97). I would refer Dr. Axe to a recent post by University of Chicago Professor Jerry Coyne, in which he endeavors to summarize the entire theory of evolution in a single paragraph. His concluding point is as follows:
“Finally, the “designoid” features of organisms - the features that make them look so well adapted to their environments and lifestyles - are the product of natural selection: the combination of a random process, mutation, that generates genetic variation without regard to whether it’s “useful” or not, and a deterministic process, selection, that winnows the variation by retaining those mutations that are better able to make copies of themselves and eliminating the worse copiers. There are other important processes of evolutionary change, like random genetic drift, but only selection can produce the design-like features that so excite our wonder.”
There you have it. Natural selection doesn’t generate “inventions” (or biological innovations), because that’s not its job: that’s the job of mutation. It may be objected that Coyne is not typical of all evolutionary biologists; however, the respected evolutionary geneticist Allen MacNeill of Cornell University, whose perspective on evolution is very different from that of Coyne, agrees with him on this point. In a 2009 blog article titled, “Can Natural Selection Produce New Information?”, MacNeill points out that natural selection has three prerequisites, one of which is Variety, generated by the “engines of variation.”
He continues:
…[T]he real dispute between evolutionary biologists and “intelligent design” supporters is not over natural selection per se, but rather the properties and capabilities of the “engines of variation”. I have written extensively about these here and here."
“Yes, natural selection … is conservative not creative. It produces no new genetic nor phenotypic information, which is why Darwin eventually came to prefer the term “natural preservation” rather than “natural selection”. However, it is also clear that the “engines of variation” - that is, the processes the produce phenotypic variation among the members of populations of living organisms - are both extraordinarily creative and extraordinarily fecund. The real problem in biology is therefore not producing new variation, but rather limiting the production of new variation to the point that the “engines of variation” do not cause the inevitable disintegration of living system…”
Not sure this is fair, Dennis. Behe has replied to this, pointing out that his case is based on the observation of what mutations have in fact occurred in the development of chloroquine resistance since it was introduced, and the frequencies of that resistance in comparison to the number of mutations that have, de facto, occurred.
Simultaneity has no bearing on his case, which is as I understand it historical.
Behe uses the concept of Devolution … which makes the very foundation of his views rather untenable.
Is a snake a de-volved reptile or a de-volved amphibian?
Is an amphibian a de-volved fish? Or a de-volved tetrapod?
It’s completely subjective… and the whole discussion about Design suddenly wobbles on the issue of Subjectivity.
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What actual observations did Behe cite?
I believe that Dennis is being more than fair. The fairest reading of Behe is that he didn’t even bother to read the relevant primary literature (the observations) in the field–he based it primarily on misreading or misrepresenting an awkward sentence from a review.
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Does this text provide any assistance?:
From the Beginning, the Critics Mischaracterized Behe
The critics were wrong from the outset. Behe’s argument in The Edge of Evolution didn’t depend on whether chloroquine resistance arose in a stepwise manner, or only after multiple mutations accumulated. His argument was based upon an empirically observed data point from public health studies which found that chloroquine resistance arose in about 1 in every 1020 organisms. He had a strong citation for this empirical observation: Nicholas White, “Antimalarial Drug Resistance,” Journal of Clinical Investigation, Vol. 113: 1084-1092 (2004). He called the mutations (whatever they were) that caused chloroquine resistance a “chloroquine complexity cluster” or CCC. Whatever molecular mechanisms may be behind a CCC, empirical data showed that 1020 cells are required in order to produce one. Behe pointed out that if a trait required the molecular equivalent of two CCC’s before providing any advantage, then that would pose major problems for Darwinian evolution.
It’s a simple calculation. Behe observed that if 1020 organisms were required to obtain one CCC, then the square of that amount – 1040 organisms – would be required to evolve a trait that required two CCC’s before providing any advantage. However, as Behe observed, a total of only 1040 organisms have lived on Earth over the entire history of the planet.
As Behe put it:
Recall that the odds against getting two necessary, independent mutations are the multiplied odds for getting each mutation individually. What if a problem arose that required a cluster of mutations that was twice as complicated as a CCC? (Let’s call it a double CCC.) For example, what if instead of the several amino acid changes needed for chloroquine resistance in malaria, twice that number were needed? In that case the odds would be that for a CCC times itself. Instead of 1020 cells to solve the evolutionary problem, we would need 1040 cells. Workers at the University of Georgia have estimated that about a billion billion trillion (1030) bacterial cells are formed on the earth each and every year. … If that number has been the same over the entire several-billion-year history of the world, then throughout the course of history there would have been slightly fewer than 1040 cells, a bit less than we’d expect to need to get a double CCC. The conclusion, then, is that the odds are slightly against even one double CCC showing up by Darwinian processes in the entire course of life on earth.
(Michael Behe, The Edge of Evolution: The Search for the Limits of Darwinism, p. 135 (Free Press, 2007).)
Hi George - if Behe is squaring probabilities, he’s calculating the probability of simultaneous mutations. That’s what the squaring does.
Put another way - if Behe was ok with evolution accumulating change one mutation at a time, then he could never find an edge to what it could accomplish. He’s looking for an edge, and he’s basing it on simultaneous mutations.
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And so, his math is clearly ridiculous.
I was wondering what was wrong with his math. Thank you for explaining it so simply and quickly.
You can look at the PubMed entry for that to see that it is definitely NOT a citation of an empirical observation. It’s a review, and Behe quote-mined it. IIRC, the author does not agree with Behe’s mathematical misinterpretation of the mined quote.
Again, as shown dramatically in the Dover trial, Behe doesn’t bother to read the primary (empirical) literature.
That’s in addition to his generalizing to all of biology from a tiny number of cherry-picked cases. His number for one of those cases (HIV) not only had no citations to support it, but was off by a factor of infinity:
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George
You might have done better had you seen this discussion of a paper interacting with him by Behe himself from yesterday, rather than a report about him. No doubt it wasn’t then available.
The first thing I note is that his opponents are interacting with his work directly, rather than drawing conclusions from reports about it. And they’re also willing to interact with him directly.
The second is that they repect him enough to admit errors in their critique of his work, rather than concluding that everything he says is proof of laziness and incompetence. That they are population geneticists who “have the maths” and he is citing empirical research makes that a good example of scientific humility and charity. That is a model I would like to see imitated rather more on this Christian site.
The third is his own closing response to those he continues to believe in error:
Here’s a final important point. Genetics is an excellent journal; its editors and reviewers are top notch; and Durrett and Schmidt themselves are fine researchers. Yet, as I show above, when simple mistakes in the application of their model to malaria are corrected, it agrees closely with empirical results reported from the field that I cited.
Here we have, in Behe, a Christian and a theistic evolutionist. And also one who is courteous and respectful to his opponents. As indeed are his secular opponents in this case. Maybe we could benefit from imitating that here.
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