Because enzyme activity is a continuous variable. Besides, what exactly is a standard antibiotic dose?
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Actually, he doesn’t. Nothing in that passage explains the lack of enzymatic assays. If you disagree, please explain in your own words.
You’re not reading carefully. Axe’s assay was survival–binary. The assays he didn’t do (and he could still do tomorrow) are enzymatic assays–not binary.
Surely, if you worked in computer science, you understand the difference?
Art wrote:
“This is probably why Axe has declined invites to join us, and will likely never, ever join a discussion with any of us, or with people who are informed about these matters.”
What you cut/pasted without understanding does not constitute discussion.
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This is why I asked you to read for comprehension. Clearly Art meant experiment. If you had any interest in understanding our position (only then can you meaningfully criticize it), you would have been able to work this out for yourself and don’t need it pointed out to you.
Try harder.
Ahh so by implication you, too, can see this is actually a problem and you don’t know how to defend it, so as I expected this is going to be your ultimately fallback every time you run into a problem. You don’t have a meaningful answer so now “if that was really a problem reviewers should have caught it, they didn’t so Axe must be right.”
Sorry, not gonna work. Every time you feed us this pathetic fallback it just goes in the “he doesn’t know how to respond” bin. And we can conclude that you too recognize that there really is a problem here that you don’t know how to defend, so better throw it on the peer review retort.
Rather transparent I think.
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I explained that. Heck, Axe explained it when he described what his goal was: “to assess the minimal constraints for proper enzyme function”
The miminal constraints for proper enzyme function. The minimal. Smallest. Lowest. Weakest. The absolutely smallest factors necessary for a functional enzyme. And in an evolutionary context that would be the smallest degree of enzyme function that natural selection can act on. That’s why you find the lowest concentration of antibiotic that measurably affects fitness. Because at such a low concentration of antibiotic bacteria don’t immediately die, so even very weak enzymes that still technically function can give a small fitness advantage.
If you had read for comprehension to begin with we could have skipped this two-post exchange and moved on.
It’s certainly more laborious, since you have to now do both growth and enzyme kinetics assays. But it’s not that this is really “difficult” work. It’s the sort of work one would expect to be done by a person who believes in their own work and is trying their best to convince the broader scientific community that they are really on to something.
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Which highlights the uselessness of ID. Just like creationism, all they tend to do is criticize science they dislike offering nothing of value to scientific inquiry, while also acting as a gateway to conservative Christianity and associated nationalistic policies.
Publishing piles of pseudo-sci books to pander to conservative Christians is not something I would be lauding as admirable.
Exactly. They have not written letters to journal editors and caused articles to be retracted.
There is that hypocrisy of yours again.
Bechly’s challenge was, in fact, answered within a day on this very forum. Isn’t that funny?
One of my comments in that discussion now seems prescient:
Three years and counting…
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It’s very odd, you are correct, they don’t have a section for notes and comments! Their web page does have a link for feedback, but that doesn’t seem to be what I was expecting. It is though, usual for a journal to have a place for notes and comment and discussion of articles, Nature has an Opinion section, Science has a Commentary section, it’s a mystery to me why you all seem to think this is not usual.
It makes perfect sense, he set out to categorize enzymes as fit, or not fit. The natural thing to do then is to choose a threshold for fitness, as he did.
But I’m not just parroting Axe, as in the comment above, where I say why I think what he did was reasonable. And I mentioned previously that Axe has published papers since 2004, one in PLOS, and is back in the lab at Biola, presumably to publish more results. I expect you all would reject the papers he published in Biocomplexity out of hand, without investigating them, so we’ll have to leave it at that. Also, the Discovery Institute, where he was before Biola, probably doesn’t have lab facilities like Biola, which would explain why the lab results stopped for a while.
The difference is that you can’t assume anything about the creation/innovation rate of a free agent.
Not sure to grasp your point. Can you elaborate ?
I’ve asked Grok how Bechly defined a new body plan. Here is the answer:
How many in peer-reviewed journals other than their own?
For that matter, how many in their own journal? Isn’t that output pathetically low?
Books aimed at credulous laypeople like you, not at working scientists.
Has any scientific paradigm changed using this approach?
Is the DI approach aimed at science or at soliciting donations?
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Actually, in the case that was described in the Panda’s Thumb article, function was restored, where part of the gene that had that previous function was present: “The rescue of E. coli ΔguaB represents a partial self-rescue; it was rescued by the hybrid YdjO257/GuaB283, a combination of 257 amino acids of YdjO and 283 amino acids of GuaB. The full length GuaB is 488 amino acids, meaning that ~60% of GuaB, fused to an almost full length YdjO (267 amino acids), seemingly performed the function of GuaB.” So this is not a new function.
Now you also need to demonstrate that gene fusion is the normal type of mutation that natural selection has to operate on, I think it’s actually rare, and changes in residues within a gene is the usual form of mutation.
Yes, he did, and he explains why, did you in fact read his explanation? He makes several points in reply, none of which you have addressed. Here is an excerpt: “Evidently we have made a mistake, because mutants that ought to be readable according to our calculation clearly aren’t readable. As you may have guessed, the mistake is that the 2-in-7 typo rate was tolerable only because it was restricted to a narrow section of seven positions. The fact that the remaining 35 positions were without error compensated in large measure for the errors in the mutated section.”
“The remedy is to use a different starting sequence. Specifically, we need the starting sequence to be of the same quality that we intend to require of mutant sequences in order for them to be accepted. Otherwise the mismatch in quality will skew our results.” This is under the heading “Objection 3 Because Axe measured mutational sensitivity from a weakly functional starting sequence rather than the fully functional natural enzyme, the mutants he generated were inappropriately disadvantaged, and this is why he arrived at such a low value for the prevalence of functional sequences.”.This was your point, now you need to reply to Axe’s extended reply to this.
By the way, where is Art, the author of the article that set out to refute Axe’s paper? Why does he seem to have vanished? So that someone else needs to take up the task of defending this…
I moved this thread to Side Convo. Have fun storming the castle! 
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First, I don’t see how an unchanging probability of creation falsifies it. And assuming a basically constant probability of evolving a body plan doesn’t seem to be the essence of Bechly’s point. He is arguing that most appearances of new body plans occur in the fossil record in windows of 5-10 million years, yet we don’t see this in a similar time frame in living species. But are you arguing that the probability can change substantially? What process can you propose for the evolution of new body plans, other than the standard NeoDarwinian narrative of mutation and natural selection? Which is generally assumed to be constant throughout geological history.
I heard someone recently make a comment about “the artifact hypothesis”, paleontologists even have a curve they show, where as you sample more and more, you will tend to more and more find items you have found in previous sampling. Until eventually the curve flattens out, and you gain confidence that you have pretty much gotten a good idea of what is out there. And this I found in a refutation of a creationist textbook, here: “Advocates of the artifact hypothesis say that the Cambrian explosion is not real; it is only the result–or an “artifact”–of having too small a sample of fossils to work with.
Explore Evolution, p. 30
No paleontologists say this about the Cambrian explosion. Explore Evolution does not cite references for this claim, but any casual examination of the peer-reviewed literature about the Cambrian explosion will fail to turn up a single instance of a paleontologist claiming the Cambrian explosion was ‘not real.’”
So do you have evidence that we are still finding new samples, enough so that we can conclude we haven’t yet sampled enough?
“A body plan, Bauplan (pl. German: Baupläne), or ground plan is a set of morphological features common to many members of a phylum of animals.[1] The vertebrates share one body plan, while invertebrates have many.
This term, usually applied to animals, envisages a ‘blueprint’ encompassing aspects such as symmetry, layers, segmentation, nerve, limb, and gut disposition. Evolutionary developmental biology seeks to explain the origins of diverse body plans.” (Wikipedia)
So presumably the developmental biologists have a good idea of what they mean by a body plan, or there wouldn’t be any such branch of science.
You need to read further. That response of yours is of literally zero value given the remaining contents of my article. Is it too much to ask that you read it to completion before posting?
You don’t read for comprehension. You don’t read to completion. What’s next, we’re going to have to teach to you read from the beginning too? To spell?
Gene fusion is not a mutation, it is a result of mutation. Insertions and deletions are the mutations that lead to gene fusion. Coincidentally a gene fusion occurred as an accidental byproduct of the insertion-mutation that resulted in the Cit+ trait in the Lenski long-term evolution experiment with E coli.
As you can see in this figure, the duplication (a chromosomal segment containing the end-part of the citG gene, and then inserted into the rnk gene, resulting in a fusion protein):
It isn’t known whether this new fusion protein has any function (this specific one doesn’t have to, it merely shows by example that such results occur from deletion/insertion mutations), it doesn’t contribute to the Cit+ trait in any case. But this is a bona fide exampel of an insertion mutation creating a new fusion protein.
If you want an example where such a mutation was directly recorded in an experiment to result in a gene with a novel function, here is a couple:
In prokaryotes gene fusions of this sort typically originate from transposable element activity, or “insertion sequences” as they are called, which are highly prone to get copied and insert themselves in various locations across the genome. They’re actually highly abundant types of mutations.
You can simply google for known examples of novel fusion proteins with new functions formed by such mutations. There are many known. And there are many review articles detailing the many known types and their activity.
There is no such thing as THE rate of insertion/deletions mutations. They can vary massively depending on species and environmental context. Some species carry very few transposable elements, others carry many thousands, and their activity spans order-magnitude ranges from 10-8 to 10-3 insertions per element.
Turns out it isn’t, really. Tell Axe his “less prevalent than previously assumed” was wrong.
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I think that’s a you-problem. Give it another go.
Edit: Okay, I was asking too much. Let me help:
Just one way in which we can explain the observation that body plan changes were prevalent earlier in evolution, but much more improbable now, is that the probability changed from high to low over time. From high probabilty in the past, to low probability in the present.
Yeah I know, this is like being cognitively assaulted by God himself with informational overload.
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Sorry I scolded you for vanishing, thanks for your reply. A quick search for “the plating assay” turned up this comment: “Applications: Spot plating is widely used in microbiology for studying antibiotic resistance, metabolic capabilities, and other microbial behaviors.” So this would not be useful for studying antibiotic resistance etc. if many factors can get in the way, and obscure the causes. Do you have evidence that Axe did not take proper precautions?
Again, I note that he has, and punting on this is not at all a good reply.
Yes. To completion. That’s how I concluded it was obfuscation. And I succeeded in explaining why.
I did in fact address it. But to understand why you need to engage in comprehension. Thinking.
But they were not without error. The “remaining 35 positions” were pieces of his temperature sensitive enzyme (in his actual experiment), not the wild-type.
Thus their capacity to compensate for the additional errors in the mutated fraction is reduced compared to that of the wild-type. The wild-type enzyme has a higher to capacity tolerate the mutations that occur in the mutated section. The wild-type enzyme has an increased buffering capacity.
Do you understand what I am saying? Axe has ALREADY mutated his “reference sequence”. I have his paper on my computer, do you want me to quote you directly his method for creating the temperature sensitive mutant enzyme that already has “errors” in it?
Do you understand what I am saying?
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Well, here is an excerpt from Bechly’s reply to you: “A more important point is the fact that the differences among the species of Hawaiian Silverswords are all related to different growth forms and allometric shifts of already existing structures. Even though the differences appear superficially striking, they do not involve any novel body plans (i.e., no new proteins, new tissues, or new organs).” Where then, does he assert that all angiosperms have the same body plan? Bechly continues: “If the different growth forms of Hawaiian Silverswords really represented different body plans, they would not have been classified in the same family and subfamily as their continental tarweed relatives, and, in the case of Dubautia, even within the same genus, at least not prior to the cladistic revolution in the 1970s when typological thinking still prevailed in biological systematics.” Further, he says: “My judgment that these plants do not have very different body plans, in spite of their often strikingly different growth forms, is also supported by the fact that they still frequently hybridize without sterility (Carr & Kyhos 1981, 1986; Carr 1985, 1995; Baldwin et al. 1990; Baldwin 2006). I can only repeat myself: organisms with different body plans cannot successfully interbreed. It is a common Darwinian dogma that new body plans correlate with significant genetic changes in early development (John & Miklos 1988: 309; Van Valen 1988; Thomson 1992: 111; Arthur 1997: 14+21; Kalinka & Tomancak 2012; Willmore 2012; Meyer 2013), which arguably would prevent any hybridization.”
By “a free agent” do you mean God? Well of course you’re right. You can’t do science at all based on the hypothesis of an omnipotent being with no constraints on what he would or would not do. It’s just surprising that you would consider this a good thing. Still, we can note that it’s very odd: if the goal was to produce exactly the current biota, why take such an exceedingly long and twisty path to get here, especially the various mass extinctions?
We don’t see most of evolutionary history in the fossil record, and we can’t distinguish ancestors from cousins. So how does Bechly determine that whale evolution took 5 million years? Notably, that sentence in his “challenge” has no citation. There are however clues that he ignores, the many whale species intermediate in morpohology in various ways between Indohyus and Basilosaurus, his two end points. And if the fossil record is as fragmentary as we know it is, these are just various twigs of the early whale tree, not any sort of main trunk.
Please don’t. Do your own work. But I note that Grok uses ferret and sea otter as an example, which if correct answers Bechly’s challenge right there. Is Grok confused or is Bechly confused?
I will also note that Grok, like Bechly, mentions a counter-current exchange system as in whales, but of course that’s in modern whales; we have no idea whether ancient whales had one.
So basically, that “definition” is useless.
True for whales also.
How does that follow? This is another extraneous criterion that can’t be determined based on fossils.
If you will note, “body plan” means something different in those references from what Bechly means.
Well, I explained why a continuous variable needs a threshold to give a way to classify enzymes as either functional or non-functional. Why did you not address this? And I meant something that would give something like the “low selection threshold” that Axe spoke of, as opposed to the absolute minimal dose Rumraket seemed to be proposing. Just a dose researchers would normally use to detect function.