T-URF13: Irreducible complexity without Intelligent Design
A comment from Arthur Hunt to: 'More On T-urf13 - A response to Arthur Hunt'
Epilogue (MN): T-URF13 is a ligand-gated pore forming receptor protein evolved in cultivars bred for male sterility called Texas cytoplasmatic male-sterile maize (cms-T maize). This amazing protein comprises a highly complex system that anti-evolutionists describe with the buzzword 'irreducible complexity'. As it turns out, it arose de novo within less than a hundred years from two fragments of the mitochondrial genome (mtDNA) of maize that do not contain a protein-coding reading frame, and obviously never did (see Hunt 2007, Hunt 2019 and Beyer, Hemminger & Neukamm 2022).
This proves that the anti-evolutionist's statement, whereupon 'irreducibly complex' systems consisting of more than two 'fine-tuned' elements could not evolve by 'Darwinian' mechanisms, is wrong. Of course, it didn't take long till the anti-evolutionists tried to refute this example by using several pseudo-arguments. A remarkably unqualified response is given by 'Jonathan M.' from the dubious ID propaganda mill 'uncommon descent' Arthur Hunt already responded to. To ensure that Prof. Arthur Hunt's reply does not one day disappear into nirvana, it is reprinted here.
Response by Arthur Hunt
Thanks for your continued interest in my essays. Getting to your latest (in order):
"I have distilled the objections down to three headings. These are:
Um, I really don't care about pots, kettles, and the like. The fact is that well-understood bio-chemical mechanisms are involved in the origination of T-URF13. Recombination has been studied for decades, and we know enough about the enzymes to know that the attendant chemical mechanisms are all that are needed to promote the genomic shuffling that gave rise to T-URF13. If you don't believe me, then you are welcome to call upon the research litera-ture, and/or study the enzymes in the lab, and point out evidence that argues otherwise.
"Again, what is being discussed is the causal sufficiency of random (that is, unguided) processes in accounting for the de novo gene (in this case, T-URF13): Did ample probabilistic resources exist in order to justify attributing such an event to chance? It seems fairly clear to me that they did not. Let me re-iterate again: A demonstration of molecular homology or common ancestral derivation is not, in and of itself, a causal explanation."
Well, when we have a good understanding of the enzymology that underlies the homology and origination of T-URF13, I would say that we do indeed have a causal explanation.
Are you claiming that there is evidence that suggests that recombination did not give rise to the gene encoding T-URF13? If so, some pointers would be appreciated.
"The Uncommon Descent writer and commenter 'PaV' made note of one or two things which I had neglected in my original piece."
PaV's contributions fall short of any sort of refutation of my points. Without quoting extensive-ly (refer to the original post for details) but instead following PaV's numbering:
1. The mode of inheritance of mitochondrial genes has absolutely nothing to do with the issue here - that T-URF13 arose via well-understood processes that do not involve ID and that defy the claims that such proteins and systems require probabilistic resources far in excess of what was available.
2. As I explained in the essay on T-URF13, Behe's own "derivation" equates a CCC with a small-molecule binding site (that would be the site to which the antimalarial binds). To argue that a polyketide binding site is not analogous to an antimalarial binding site makes no sense to me. (The fact of the matter is that a polyketide is much more like an oligopeptide than is chloroquine.)
3. The concept of "Darwinian" recombination is an odd one indeed. Recombination is cata-lyzed by enzymes. Period. Whether it happens in the nucleus, organelle, or cytoplasm (or anywhere else) is quite irrelevant, and the location of the genome (and events) in question has no bearing on the fact that the "probabilistic resources" provided by the process fall far short of those demanded by ID advocates. In spite of this, T-URF13 exists.
4. I invite PaV (and Jonathan M) to read the entire paragraph and section of the review from which Behe pulls the 10^20 number. I've discussed this matter elsewhere, and will just state the obvious (well, it's obvious if one has access to the complete article, and not just to Behe's book) - this number is at best only distantly-related to the events needed to generate a "CCC".
5. The stuff about "de novo" genes is not relevant to T-URF13. I ask that you go back and read all of my essays on the subject.
6. Nuclear restorers are near and dear to my heart, as they are usually RNA-binding proteins that have evolved to acquire new RNA sequence preferences. These new functionalities promote the degradation of T-URF13-encoding mRNAs. (To state things in a way that will perk up the ears of readers here, they have acquired new functional information. And without design. Go figure.) Why PaV thinks that these in some way deflate the reality of the T-URF13 example escapes me.
Finally, PaV's comments about the physiological consequences of T-URF13 expression tell me that he (and, I presume, most ID proponents) does not think much about the creative pos-sibilities attendant with apoptotic processes, and on top of that that females are evolutionary dead ends. Neither of these opinions makes any sort of biological sense, and I don't think that this sort of nonsense has much of an impact on my arguments. (T-URF13, in a nutshell, is a gene that converts a hemaphrodite into a female. This sort of evolution is seen in the wild and is one of the many fascinating reproductive strategies that plants have evolved. The toxin sensitivity is an afterthought and serves to illustrate that, in biology, it is almost impossible to find a trait that is exclusively, back-or-white, beneficial or detrimental.)
"Arthur Hunt provides a link to a blog where he critiques the Axe (2004) paper which I cited regarding the prohibitive rarity of functional protein folds with respect to the vast sea of combinatorial sequence space."
I ask that you take your time and understand all of the points I raise in my review of Axe's work. The criticisms you raise here are addressed in the essay, such that they render your points irrelevant. I will wait for your promised post on my essay to elaborate (or not, as I am hopeful that you will understand why my assertion is true).