No. He’s been trying to argue that is what he did (introducing various misleading measures of “realism” into his experiment), but the statement isn’t actually true. The way he designed his growth experiments it is literally impossible for it to inform any “edge where selection can start”.
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Can you show me where he made this claim?
In the 2004 paper. Have you bothered to read it?
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How would you design the experiments differently?
Let’s lower the temp just a bit, we’ve been here before, ad naseum so let’s try to find new ground or common ground (heaven forbid). As always, avoid the personal.
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I would suggest that this exchange represents a potential breakthrough:
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In nature, bacteria aren’t selected for A) the ability to generate colonies visible to human researchers on agar plates in a matter of a few weeks or months. They’re selected on B) their ability to survive and reproduce faster than their competitors, or where their competitors can not. So what makes for a selectively useful enzyme in case A is not particularly informative with respect to B.
So to really get at where selection might start to act in nature on enzyme activity, you’d measure enzymatic activity of a lot of mutant enzymes, give very low activity enzymes to bacteria and do growth competition experiments using carriers of active enzyme vs carriers of inactive (but still expressed) enzymes(to filter out the effect of the cost of expression), at antibiotic concentrations well below MIC. You’d have to find the lowest concentration of antibiotic that measurably reduces growth-rate of your bacteria, without actually preventing their ability to live in the medium.
If the active enzyme gives a competitive growth advantage then it is selectively useful within the range of population sizes and antibiotic concentrations achievable in the experimental settings.
Make lots of mutant enzymes to find the one with the lowest possible activity that still measurably gives a competitive growth advantage vs carriers of fully inactive but expressed enzymes. That would be a much more plausible edge of selection for enzyme activity in nature.
Now in reality, enzymes are much more likely to evolve as low-level side activities from other proteins with useful functions(usually already existing enzymes with moonlighting side-activities). It is their already existing functions that ensure their continued expression. Unsurprisingly TEM-1 Beta-lactamases are thought to have evolved from much older DD-transpeptidases, instead of by some sort of de novo fold-emergence in the way Axe tries to make it appear.
There are other problems too with his experiment. But this is specifically an issue with his idea that he’s testing the edge at which selection might start to act on activity. He most assuredly is not.
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Where do you think an environment like this might exist in nature that allowed the wild type of beta lactamase to evolve by natural selection and then be able to survive a human prescribed dose of penicillin?
.
On a classic ID the Future episode, Dr. Dominic Halsmer, a Senior Professor of Engineering at Oral Roberts University, discusses his peer-reviewed paper, “The Coherence of an Engineered World,” published in the International Journal of Design & Nature and Ecodynamics .
Is there a scientific hypothesis in paper?
Innumerable environments in nature are like this. Take things like soil or aquatic environments. They contain a large diversity of microorganisms, including both bacteria and fungi, and different places will have different representations of species depending on what food sources exist. So you’ll get zones with different bacteria, for example around the root networks of plants you’ll get a special distribution of bacteria. And top soil will have a different distribution. And fungi and so on will be working on decomposing plant matter yadda yadda.
So basically in one place you’ll have a lot of bacteria, and in a nearby location lots of fungi. The fungi will express their penicillin-like antibiotic compound, and these will diffuse into the environment around them, and some location slightly further away there’ll be a very low concentration of this antibiotic diffusingi in, and in this zone of low concentration is where bacteria will evolve antibiotic resistance because it’s low enough for them to survive in it, yet high enough for it’s effect on competitive growth to give a selective advantage to those that carry resistance-conferring mutations, for example by mutations that enhance a very low side activity of some other already existing enzyme with another useful function.
Bacteria can survive in many places on the human body in places where antibiotics you take orally never rise to high concentrations. For example on your skin. Alternatively someone is using their prescribed antibiotics incorrectly, leaving surviving microorganisms with increased resistance behind that were never eradicated.
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That’s a weird title for a journal. Is it real?
It seems to be a mashup of fine tuning with a wandering survey of the familiar ID collection of design exemplars. This quote from the paper may be taken a reflection of its scholarly quality:
When the propeller was first engineered, the developers found the basis of their design by looking at a cell and analyzing a flagellum. Scientists and engineers then used reverse engineering to discover how the flagellum was able to produce movement of the cell and applied these principles to largescale systems that we now use for transportation.
!?Huh!? The propeller, like many engineering developments, is the result of refinement of the technology over generations. Key figures go back to Archimedes, through Bernoulli as all things fluid dynamics, and was well known enough to feature on the revolutionary war submersible the Turtle. The propeller existed in roughly modern form well before detailed study of bacterial flagellum. Here we have ID progressing from an already fallacious argument from analogy, to full on delusion where they appropriate the analogy to rewrite real world history to fill in the backstory.
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No.
Curious that EN would be talking about a 12 year old paper in a very obscure journal that makes no scientific argument whatsoever. It is, however, the first “paper” I have ever seen that cites The Design Matrix.
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@colewd, are you thinking that doctors prescribe doses of penicillin that are higher than the levels that a colony of Penicillium might produce in the wild? Why would you think that?
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It is published by the Wessex Institute of Technology (which I’ve come across before and not in a good way), which appears to have a bit of a reputation as a predatory publisher, and has published a number of pro-ID papers in the past.
Doctors prescribe doses that will rid the patient of the infection. I don’t think the argument is credible that the sequence that generates beta lactamase was created by nature through a trial and error process.
I’m just trying to deal with the phrase “classic ID the Future episode.” That’s really stretching the meaning of “classic.”
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Sadly what you find credible is no indication of what has occurred in history.
The evidence implies that beta-lactamase enzymes evolved from proteins with a similar structure acting on similar substrates.
https://www.sciencedirect.com/science/article/abs/pii/S1368764604000184
They don’t appear to have been wished into existence, nor to have sort of formed by the kind of blind spontaneous polymerization tornardo-in-a-junkyard strawman creationists always try to make evolution appear like.
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Art didn’t offer an argument. He asked a question that you appear to be unwilling or unable to answer. Why is that?
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It is a scientific hypothesis. However, I do not see how this is intrinsically related to Intelligent Design.
How does the idea of Intelligent Designer lead ineluctably to the idea that protein functions are rare and isolated in sequence space?
Isn’t it completely plausible that an Intelligent Designer could come up with a way of designing sequence spaces and protein functions such that protein functions would not be rare and isolated?
EDIT: I in fact believe that God is intelligent, that He has designed the universe including protein function, and that (based on biology literature discussed throughout on the forum) that protein function is not anywhere close to the rarity and isolation hypothesized by Axe. As such, I am living proof that belief in an Intelligent Design is not intrinsically connected to Axe’s hypothesis…
…unless…
you would want to argue that my belief set is irrational and hopelessly self-contradictory.
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