Thanks Dennis… no hurry required.
Well there is a long history of evolutionists wanting to define evolution as “change over time,” any change over time. Aside from the obvious rhetorical advantage this provides evolutionists, by defining their theory as an undeniable given, there actually are historical, non scientific, reasons for this accommodating view of evolution. I’ve written about it in my book Darwin’s God, and in my blog. It isn’t germane to this discussion, so I’ll avoid what would be a lengthy tangent.
The point here is not about the semantics. The point is that this study does not help remedy the problem of evolution constructing protein-protein binding sequences.
Well your contention that it qualifies as evolution because “it happened,” goes beyond even the accommodating “change over time” criterion. Now you are talking about “change over time, even in a highly contrived, artificial, laboratory experiment.” If we are going to find support for evolutionary theory here, I believe it is not in casting the experiment as an example of evolution happening. That would be to strip the term “evolution” of any practical meaning. Rather, I think the experiment would have to be found to provide results that can be interpreted as relieving evolution of barriers, and specifically providing a plausible explanation for the evolution of protein-protein binding sequences.
Well that is another question. I will say that too often neutral evolution is seen as a sort of magic bullet that resolves otherwise tough problems. It is no such panacea. In the absence of selection acting on the kind of fitness pathway that fortuitously was present in this study, protein-protein binding sequences are an example, one of a great many in biology, that science does not indicate would evolve. Drift is a very weak search engine. I’m not in the habit of attempting to prove universal negatives, but in a positivistic sense, science does not indicate the random evolution of things like protein-protein binding sequences.
Well again, I think it is obvious that this study does not refute Behe’s explanation of the protein-protein binding sequence problem. The experiment is a highly artificial, contrived, environment. You can set up protein evolution processes to find sequences with specific functions. But there is no correspondence with what actually could happen in evolutionary history. And if you could somehow show that a realistic evolutionary environment could make this sort of search, then all you have shown is that there are lucky cases where a binding protein can evolve to bind to a similar partner, given some fortuitous (host) mutations and a lucky fitness pathway. This just isn’t the general rebuttal that your article indicates.
If I might make a suggestion: Rather than trying to stretch results beyond their limits, it seems to me that this study provides actually a bunch of fairly interesting, if not profound, points to think about. For instance, it confirms the “all or none” view of this very specific example of protein-protein binding sequences. That, of course, is one example of a great many types of biological designs. Second, the solution path that was found involves serendipity, rather than some sort of biological process or law. Third, what about such serendipity? What if science were to discover a whole bunch more of these pathways? First, this is not indicated by today’s science. But perhaps more interesting, if such pathways were to be discovered in great numbers in the future, it would be an incredible finding. It would have great implications for our philosophy of science, the nature of biochemistry, physics, and so forth. And clearly, it would raise the specter of final causes and design. Finally, there is the suspicious finding, skipped over with brevity in the paper, that there were zero synonymous mutations in all those lineages, in the entire experiment. Why is that?
So my point here is, without even particularly advocating for evolution (or design), there is a lot of interesting stuff here to consider. Why always try to stretch the results as unequivocally confirming / supporting evolution?
Hi Cornelius - as has been mentioned several times already, protein-protein binding is hardly “all or none”. There are a range of affinities seen. It’s commonplace for biologists to observe changes in binding strength with point mutations, for example. Are you suggesting that every point mutation in a protein should abolish its binding to other proteins? What of point mutations that decrease or increase affinity? We observe those all the time.
Also, anything other than “observing the results of natural biology without interference” could potentially be derided as “an artificial environment”. I’ve seen ID arguments that basically run to this idea - anything other than a purely natural, 4.5 billion-year repeat of evolution is “artificial”. As far as the phage was concerned, this was its environment that it was replicating in. Why do you think this experiment is somehow not informative?
You are suggesting that this result - that a new protein-protein binding site came about because there was a selective path towards it - is somehow so infrequent that we should never consider it as an option for evolution.
And yet, it happened, while we watched it happen. If it’s really that vanishingly rare, how did we get so very lucky that we observed it happen?
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Hi Cornelius - this is an assertion. It’s not backed up by evidence.
We see examples in evolutionary change where neutral or nearly neutral mutations later become essential for a new function when they combine with later mutations. One example where this has been demonstrated is in the Lenski LTEE. The population that evolved the ability to use citrate in an anaerobic environment was later shown to have had a mutation necessary for this event occur thousands of generations prior. The single mutation on its own does not confer the cit+ phenotype.
For those curious to learn more about this example, you can read a post I wrote about it some time ago.
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Well you are misinterpreting the phrase. The “all or none” phrase is not in reference to binding affinity, it refers to the function conferred by whatever binding you have. This is what they confirmed in the study.
Well sure, but we’re nowhere close here. It was not an intention of the study to set up anything like a realistic environment. I’m not saying that nullifies the results. They mapped out a pathway to switching over to OmpF. That’s certainly legitimate.
Oh gosh no, these laboratory assays are about as far away from reality as you can get. This can hardly be said to be “its environment.” And this is to say nothing of the ingenious setup they arranged, where the well-fed host significantly reduced, but did not shut down altogether, the phage’s normal entry. I’ll just paste in a few sentences to give an idea of the highly artificial experimental procedure:
Again, no, not at all. I’m not saying that fortuitous events could never happen in evolutionary history. In fact, I’d be surprised if this never was observed. Especially in a case such as this. OmpF is similar to LamB, and a similar phage is known to bind to OmpF. But it is not controversial that this was serendipitous. If you want to argue that it wasn’t, and that this is the rule, then you have an argument with the authors of the paper, not just me and others. The important point here is that we are not talking about a gradual buildup of a function, but rather a different function, which fortuitously then provided a set up for the new binding, with only a single mutation required.
As I said earlier, while this is clearly serendipitous, my point is not that your idea (that perhaps molecular biology is full of such serendipity) is necessarily wrong. It is not indicated but, hey, who knows? I say keep it up, keep pushing that idea forward, if you like.
But this is not indicated by the paper. Furthermore, as I said earlier, if such pathways were to be discovered in great numbers in the future, it would be an incredible finding. It would have great implications for our philosophy of science, the nature of biochemistry, and so forth. And clearly, it would raise the specter of final causes and design.
There is just a lot more here than a simple finding. I think this is further illustrated by the fact that zero synonymous mutations were found. Why is that?
No Dennis, this is by no means merely an assertion. I suspect you are unfamiliar with the search problem. There is a reason why evolutionists pushed so hard on natural selection for a century. Without it you have an enormous problem. There is no free lunch. You can’t just turn on a random search and expect the species and their designs to come out of the other end. The fact that you would point to the LTEE’s utilization of citrate in aerobic conditions makes my point. I discussed that finding here.
[quote=“Billcole, post:180, topic:9418”]
Your analogy appears to me to compare Michael Jordan (in his prime 
) demonstrating he can jump up and touch the top of the empire state building because he has recorded a 47 inch vertical jump. The jump is impressive but it won’t support the extraordinary claim.[/quote]
There’s no analogy there, Bill. We’re talking about protein-protein binding.
[quote]This is a not a meaningful statement until you define the size of the sequence space. Since the space grows exponentially with every added component.
[/quote]The size of sequence space is very well defined. We know the number of V, D, and J segments and the size of the binding site.
You’re making the claim that specific binding requires a specific sequence, remember?
[quote=“Cornelius_Hunter, post:194, topic:9418”]
No Dennis, this is by no means merely an assertion.[/quote]
It is merely an assertion, and it’s false.
[quote] I suspect you are unfamiliar with the search problem.
[/quote]Your assertion is false on the basis of existing, natural, well-studied (in real time) phenomena.
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[quote=“Eddie, post:184, topic:9418”]
Make your argument against Hunter, not me. I’ve said nothing one way or the other about the details in this particular dispute, and won’t while Hunter is around who knows much more than I do.[/quote]
Does he?
Why would training count for more than experience and productivity?
[quote]Years ago, Dennis Venema and Kirk Durston had a great debate here on BioLogos – very polite, staying on topic, with technical competence shown on both sides…
[/quote]On what basis do do you assess technical competence?
[quote=“Cornelius_Hunter, post:193, topic:9418”]Well you are misinterpreting the phrase. The “all or none” phrase is not in reference to binding affinity, it refers to the function conferred by whatever binding you have.
[/quote]
I don’t see any misinterpretation. Here’s what you wrote:
Two mentions of binding, no mentions of function…
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Hi Cornelius - I am quite familiar with “search” issues in evolution. The evidence we have shows that searches are not a problem - whether making new protein-protein binding events, making antibodies (a subset of the former), finding new functions (such as cobbling together a citrate transporter that can work when oxygen is present) or making new species (such as humans and chimpanzees arising from a shared ancestral population.
In each case, the “search” is hugely constrained by the starting point - VDJ segments, the structure of protein J prior to mutations, the genome of the human/chimp common ancestral population, and so on.
If the “search problem” was a problem for evolution the way ID folks claim it to be, then antibodies with high affinity would never form, protein J would not be able to switch to a new receptor, and new species would not arise over time. This may well be what the ID movement would like to establish, but the evidence we have strongly supports the idea that all of these events are possible, and even probable.
At the end of the day, the assertion that protein functions are exceedingly rare in sequence space is just that - an assertion - which is usually backed up by only one paper (Doug Axe’s 2004 paper). Doug’s estimate is wildly off. The main problems are that he used a protein for which there was barely any function left (despite your claim that function is all or none, there’s an example, right in the literature by an ID proponent that shows otherwise (!)) and he made multiple simultaneous mutations (sound familiar?) to it. Guess what? The vast majority of the time this removed protein function. It simply does not follow, however, that this is a reasonable way to estimate the density of functions in sequence space.
Put another way: do you really think in an environment where protein functions are only present at one in ten to the 77th power that protein J would just happen, by chance, to have another function sitting only four amino acids away? What are the chances? That’s like picking two protons in the universe at random and finding out they are only one nanometer apart.
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@Cornelius_Hunter, your objections on these issues are pointless if you refuse to explain where millions of terrestrial species have come from since the days of Noah.
But on the other side of the coin, there are plenty of cases that work perfectly in Evolutionary scenarios from common descent! Genetic drift lays the ground work for all sorts of later mutations. The hollow bones of one particular group of dinosaurs wasn’t to allow for flight … but millions of years later… the low density of these dino’s make flight possible.
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Well your arguments and examples aren’t doing much to demonstrate your expertise, save for your human-chimp example, but that one suffers from being circular. Sorry, but you can’t assume the truth of evolution when attempting to argue that it works just fine.
Oh, gosh no. Unless you know of some ID folks that I don’t know. ID arguments do not preclude the immune system antibodies. For these vertebrate immune system antibodies, a relatively few residues are substituted, differently across a large number of antibodies, and essentially immediately tested against targets, in a continuous procedure. This is light years away from the hypothetical, glacial, evolutionary process. Your continued appeal to the antibody search problem is not helping your case.
Well you are really fighting the science here. You are heroically fighting the tide. Axe’s paper is far from the only work showing these results. This is by no means an ID conspiracy (I wasn’t even aware of Axe’s work for quite sometime). If Axe’s estimates are “wildly off,” then so are several others. Also, the “all or none” phrase comes from the paper, and is specifically directed at the protein-protein binding problem. My point was simply that the paper’s finding of such an “all or none” is no surprise.
Well now you’ve gone beyond fighting the tide. The notion that protein sequence space is that densely packed with function is, frankly, [pick some outrageous word to go here]. The problem here is that you are zooming in on the tactical, narrow, view, and then extrapolating that to a strategic, wide view. Your result is “wildly off” to use your phraseology.
Protein functionality is not limited to a single canonical sequence. There generally is a large number of tightly clustered sequences that will provide the functionality. And most proteins have multiple functions. What you are focusing in on here is even more tactical: you are looking at the few residues that influence the binding interface. With a few mutations, you can bind to a similar membrane protein (which a similar phage is known to bind to). So you have switched from one membrane protein to another, both sharing the same fold and tertiary structure. And the protein J is providing the same overall functionality, just with a different membrane protein. This in no way extrapolates to the different question of the density of protein function across the entire, astronomical, sequence space.
So back to our topic, your article incorrectly casts [Meyer, et. al., 2012, Science] as rebuking Behe, and I would still like to hear ideas on why Meyer, et. al. found zero synonymous mutations in all their protein J alleles.
Cornelius, I don’t “assume the truth of evolution”. The evidence supporting the hypothesis that humans and chimpanzees share a common ancestral population is, to put it mildly, quite strong, despite your claims against it. As such, it is quite reasonable to use that evidence to infer what evolution might be capable of, say, given 4-6 million years to work.
There are also many references in the literature that provide rather different estimates from Axe on the rarity of function in sequence space. Axe is near the extreme end of the spectrum of estimates - and his estimate is only for one beta lactamase for that matter.
You also haven’t addressed the issue that the sequence space that antibodies search is very small relative to the entire protein space - and yet antibodies form readily. How is it that all of those functions (binding to antigens) are packed into that tiny search space if Axe’s estimate is correct? As we have repeatedly pointed out, antibodies and proteins in general search the same type of space - protein sequence space. If Axe is right, how is it that antibodies find their function in that tiny space? You haven’t explained how this is possible. If the space is really that sparsely populated, no amount of “streamlining” the system should be able to overcome the vastness of that space to be searched.
But I suspect we will have to leave it here for now - life calls, and other needs are more pressing. Perhaps @Swamidass, @Argon, or @benkirk would care to continue the conversation.
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This “debate” can go on indefinitely. I really do not see its purpose.
@DennisVenema takes a position largely accepted by mainstream science. @Cornelius_Hunter does not. There are irreconcilable differences in how these two think about data, science and evidence. This conversation mirrors larger schisms between the ID movement (that has its own way of interpreting data) and those of us in mainstream science.
Of course, I have my opinions about who is “right”, but this disagreement cannot be adjudicated in this forum. This is not how scientific arguments are litigated. @Cornelius_Hunter, even if you are to “win” this argument, you will have no impact on how science sees this topic. Literally zero impact. This is a totally futile way of impacting how science is done.
Rather than pretending that this is a useful debate, I think it would be better to end this line. For those interested in the science here, rather than a debate, I think there is value in explaining how mainstream science works and why it is so certain about evolution. Disagree if you must, but there is value in understanding how mainstream science works. It is not nearly as ideological or unreasonable as some might assume.
So, I have no interest in continue a debate here of any kind. I have no interest in participating in an entirely futile effort.
On the other hand, those curious about how mainstream science works and how it comes to the conclusion of evolution, well I am happy to explain that =). Despite the fears, evolution is not an assumption of science, it is the conclusion arrived at based on a vast amount of scientific evidence. Of course, using rules other than mainstream science (e.g. assuming YEC) one will come to different conclusions.
It is clear that many people disagree with that conclusion. Great. We all know that. Our effort here, however, is to explain why mainstream science has come to this conclusion. I do not have the desire to debate it.
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You can’t argue science with people who aren’t doing science, and anyone who can’t give an age for the earth or explain the diversity of species even after Noah (let alone the entire fossil record), isn’t doing science.
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Good thoughts, Joshua.
For the record, my reason for engaging critics - even if they are well outside the mainstream - is not because I expect those critics to change their views, but that I hope to help others watching the exchange understand why their views are outside the mainstream. One danger of this approach, of course, is that it can appear to inflate the value of the critique. It’s hard to find the right balance.
I also do want critics like Cornelius to feel that they can come to BioLogos and converse with folks here. One of the things I appreciate about BioLogos is that we do welcome critical voices (sometimes, perhaps, to a fault). One reason for this is, as I see it, is that we feel the truth need not hide behind a wall that shuts out dissenting voices.
Well, time to get back to other things. Goodnight all.
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Thanks for the interchange Dennis.
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Likewise Cornelius - thank you.
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@Cornelius_Hunter is not YEC. He appears to be an old earth creationist. I can’t explain why he doesn’t just come out and say it when asked, but it seems he thinks God specially created each species. The implication that he is YEC probably isn’t that helpful.