Note this approach is exactly what happened with the Lenski LTEE. The experiment started with twelve isolated E coli colonies. Six of the colonies were clones of a founding strain called REL606. Six more of the colonies were clones of a very similar founding strain REL607. Over the course of the experiment all twelve strains were subjected to identical environmental pressures yet all twelve evolved in completely unique ways, including the famous citrate user mutation.
To me that’s a pretty strong indication there was no “front loading” in the original organisms.
When the DI talk about this signal peptide business, are they ignoring @Art’s figures 2 and 3 in his article? It seems pretty unequivocal that the sequence of t-urf13 came from the 3’ end of the 26s rRNA. The signal peptide “match” consists of 9 amino acids out of a 13-residue stretch matching the signal peptide of RLF32_ARATH, a gene found on chromosome 4 (the nuclear genome!) of Arapidopsis.
(query = t-urf13, subject = RLF32_ARATH).
I did a BLAST search for the A. thaliana RLF32 protein sequence against monocots. Note that A. thaliana is a Eudicot, and maize is a monocot. As you can see below, the protein sequence isn’t highly conserved between the groups, especially the signal peptide sequence (highlighted in red).
Are we expected to believe that the signal peptide sequence remained well conserved between A. thaliana (eudicot) and the maize (monocot), then in this particular strain of maize this 13-aa sequence jumped into the mitochondria to become part of the final sequence of t-urf13? Even if true, how does it follow that the rest of the sequence of t-urf13 was from the same source, just because the protein this signal peptide allegedly came from (RLF32) is also an ion channel?
If anything, why not mention that the first 30% or so of the sequence of t-urf13 has a few matching residues with the cytochrome b protein of Apis mellifera?
(query = t-urf13, subject = CYB_APILI).
Again with the assuming that sequence identity means common descent. It could be common design. The signal sequence could be the same which directed it to the mitochondria until it was broken and now it incorporates into membranes nonspecifically. In order to allow the toxin in, it would probably have to incorporate into the regular cellular membrane.
And anyway, even if none of that is true, it’s only supporting evidence. The rest of the argument suffices without that.
I understand that. The argument is not that artificial selection explains why it arose. It’s that it probably performed a real function prior to its appearance and devolved, as opposed to Hunt’s highly improbable scenario of serendipitous mixing and matching of various sequences for no reason.
Its authorS. And my argument is that T-urf13 invalidates any conception of design when it comes to multi subunit irreducibly complex systems. The authors most definitely do not agree.
The authors of the ENV piece are most certainly wrong.
The connection between T-urf13 and the calcium channel is illusory. This is something the authors pulled basically from out of thin air. I will go into detail in another post.
T-urf13 is not under nuclear regulation. As for function, the authors of the ENV piece make an argument that actually casts into non-existence a sizable number of plant species. Again, more detail will come in a later post.
T-urf13 is not designed, and it is not a broken protein. This claim is beyond absurd.
Patience. The authors of the ENV piece have given me a veritable cornucopia of error, misstatement, and comic relief. I do have a day job, and cannot jump right into the fray.
I really do not care. You ID people have to be tired of being taken to the woodshed, over and over and over. It is happening again.
T-urf13 is a clear “before and after scenario”. There is no mistaking this.
You want dishonesty? Try reflecting on the way the authors discussed Pring et al.
This “signal peptide” is not identified as such by the much more reliable SignalP tool. It’s identification as such in T-urf13 is almost certainly wrong.
Regardless of its relation to other proteins, a design view necessitates that most of the functional features here did not arise de novo. That is vastly improbable, probably much lower than 10^-60 due to the fact this is not a bacterial population. One would have thought you would jump at the chance to demonstrate exaptation from pre-existing features.
Why would that be? Do designers not create things with new features “de novo”? Like, say, the guy who had the idea of adding a luggage rack on top of a car?
Yet it happened, essentially in real time, by random recombination processes that are well-known in plant mitochondria.
This tells us that the arguments used to derive the 10^-60 figure are wrong. That is one the the main points. When “the math” doesn’t agree with reality, the appropriate thing to do is revisit “the math”, not consign reality to the trash bin.
This is a caricature of the ID position. Nobody is claiming God created this thing directly. The idea is this is a previously functional protein that broke and no longer performs its intended function, not a series of imagined mutations from vastly disparate functions just because of sequence identity.
Are you claiming this adaptation occurred after the maize genome was sequenced? Just to be clear.
This is your argument. You claimed tURF-13 constituted 3 "CCC"s. By definition a CCC is a cluster of mutations having an empirical probability of 10^-20. Is that not what you meant?
Well, I thought ID was a scientific hypothesis and had nothing to do with any gods. But that aside, you do not seem in agreement with Behe’s position, which is that “the designer” does create new functions by intervening at points in the evolutionary process Can you provide some of the evidence that you believe contradicts Behe’s position, and why you think he is wrong?
Seriously? You are aware that the cmsT corn has a pedigree, aren’t you? I cannot believe you are claiming what you seem to be, it is so absurd.
Actually, on ENV, there was significant revision of this definition of a CCC, and I plan on revising my own argument here on PS based on what the ENV authors proposed recently. Patience.
I’m YEC. Obviously I don’t believe God intervened as other theistic and old earth views require. In that respect I’m closer to you than Behe. But at least he doesn’t speculate about it. He lets his critics do that.
There’s an official ID position now? Last I heard there were close to a dozen, from literal Genesis to front loading to Behe’s occasional tinkerer to Meyer’s Cambrian Designer, etc. How did you determine which was the “correct” ID position?
How did you determine a previous function was “intended”? Intended by who or what? Exapation or the modification of existing features into new roles is a well known evolutionary mechanism.
That is not the definition. CCC stands for “chloroquine complexity cluster”, which is defined as any adaptive trait requiring the same number of mutations as chloroquine resistance in the malaria parasite (Why Behe chose this over any of the other billions of other genetic traits he could have chosen is one of the enduring mysteries of ID.)
The point being, the definition does depend on any particular odds of the trait arising. The 10^-20 figure was just Behe’s own miscalculated attempt to quantify how often a trait of such complexity would be expected to have evolved.
It seems you need to brush up a bit on your understanding of ID theory.
