It seems that way because Dennis has used a straw man argument so I am just returning the goal posts to the original position. Difficult and impossible are very different words.
If I used impossible in the past I misspoke and apologize.
As we explore this idea the main point is how much help is studying the immune system in helping us understand how diversity evolved? I think Dennis has surfaced a very good idea.
Hi Bill, I haven’t equated anything here - we were discussing the exploration of sequence space. The “sequence space problem”, however, is the same for the immune system as it is for evolution in general.
Did you know that the variable region of antibodies is about 110 amino acids long? That’s a pretty long chain. Random mutation and selection can easily find new protein-protein interactions within that 110 amino acid space. No problem at all.
The example I gave you earlier, which I don’t think you’ve interacted with yet, shows an example of one new protein-protein binding event, that required 4 amino acid changes. It was of huge selective benefit to the organism.
I agree this is very interesting and I would like to know more about how this mechanism works. At 110 amino acids a purely random search with one solution is out. Are their a library of sequences for the cell to draw from? Is the binding area smaller then 110 amino acids? Are the amino acids that are hyper mutated a subset of the 110 amino acid chain?
Can you make an argument that this is the result of lots of solutions in this search space? Even if you could establish that you had 10^40 ways to bind to a particular protein claiming this is a random search of 110 amino acids until the protein successfully binds is a stretch.
How much do you think this brides the gap between mutational adaption, which we all agree with, and generating a new genetic innovation like a flagellar motor?
[quote=“Billcole, post:90, topic:9418”]
It seems that way because Dennis has used a straw man argument so I am just returning the goal posts to the original position. Difficult and impossible are very different words.[/quote]
I disagree.
I was paraphrasing. Here’s your claim:
Your premise is simply, utterly, empirically false. Why did you make such a claim?
[quote]As we explore this idea the main point is how much help is studying the immune system in helping us understand how diversity evolved? I think Dennis has surfaced a very good idea.
[/quote]You’re trying to make it something that it is not. It’s simply a direct, factual refutation of your false claim quoted above. Your claim was only about binding, see?
Ben please support this claim that what I said is empirically false.
[quote=“Billcole, post:94, topic:9418”]
I agree this is very interesting and I would like to know more about how this mechanism works. At 110 amino acids a purely random search with one solution is out.[/quote]
Has that not been made clear to you yet, Bill? How is it that you keep overlooking the essential and nonrandom role of selection?
Yes, but you’d need to learn about recombination and abandon your focus on mutation to grasp this major source of variation in this system (and in evolution).
Areas are 2-dimensional. This is 3-dimensional.
[quote]Even if you could establish that you had 10^40 ways to bind to a particular protein claiming this is a random search of 110 amino acids until the protein successfully binds is a stretch.
[/quote]That’s not what is being claimed.
First, you need to distinguish between fact and speculation.
Please support this claim.
If you immunize genetically-identical individuals with the same antigen, then select and clone the B-cells producing the antibody, the V regions have different sequences.
This is done every day in the process of making monoclonal antibodies. It’s the foundation of an enormous amount of medical diagnostics. It was in undergraduate immunology textbooks 30 years ago.
Thus, your premise that “specific binding requires specific sequences” is objectively false. Does that change your position?
Might that make you think about why Axe and Behe don’t mention this?
It’s not mere conjecture. The DNA evidence is of the same type and strength that we use to observe legally that “Billy Bob is the father of this child (a past event), Bobby Joe isn’t.” Do you object to those too?
Hi Eddie,
Your formation, in that you arose from gametes from your two parents, is an unobserved past event. Nonetheless I would be quite confident that if I sequenced the genomes of your two parents, I would find evidence that would be convincing to all that you did indeed arise through this process. Presumably you wouldn’t have a problem if I said, upon sequencing your genome and those of your parents, that in your mother’s cells a specific crossover event took place here, or there; likewise for your dad, etc. So the issue isn’t speaking concretely about past, unseen events - it hinges on how reliable you think the evidence is.
Ok, let me put it this way: the enzymes that do VDJ recombination in vertebrates bear an uncanny resemblance to transposases, and they even are able to function as transposases (!). Why might that be the case, do you think? Could it be that they are exapted transposases from mobile DNA? Biologists are convinced, even if that “convinced” state is always open to advances in knowledge.
Another example: I have no problem saying “humans and chimpanzees descend from an common ancestral population.” Should I forever couch that in subjunctive prose, and never the indicative? Your complaint seems like a dressed-up version of the “were you there?” rebuttal.
Evolution of proteins happens in the protein sequence space; antibodies are proteins. They’re exploring the same sequence space.
Hi Ben
I think your criticism is fair. I will change my position to a specific range of sequences.
If you’re interested in the nuts and bolts of immunology there are plenty of resources available online. I’m sorry but I don’t have the time to teach you this information, unless you sign up for a class at TWU. 
The question you need to wrestle with is this: yes, this is a random search, and yes, it works incredibly well. Why might that be the case? What might it tell me about protein sequence space?
On the lambda J / OmpF interaction, did you know that Behe claims that this number of mutations (4 amino acid substitutions in this case) is beyond the reach of evolutionary mechanisms?
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.
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.
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