Seriously, who can I ask about what in my post was objectionable? I see nothing, and therefore can’t fix it.
Are you sure about that? Dr. Harshman seemed to question that point.
Not sure what you’re referring to?
They’ve not been shown to be incorrect, how about the evolution from Lentis Retractor muscles to Ciliary muslces.
Thanks for you input, but skin tissues are more opaque than lenses, and the issue of nuclei and organelles being absent in lens cell types IS in the literature as an important feature of its function. The word “transparent” can be removed. The fundamental problem stands, and you and others have help me word my case in a way that makes it more forceful.
So I thank you for your editorial suggestions.
One of the steps is formation of certain critical proteins and protein complexes. Joe Deweese, associate professor of biochemistry at Lipscomb and adjunct professor at Vanderbilt school of medicine help me enumerate the challenges of evolving Topoisomerase. This is one of the steps on the Stairways to Understanding:
The above is a more advanced Topoisomerase, Topoisomerase II, but it had the nicest picture.
Topoisomerases are a family of enzymes that manipulate the topology of DNA.
The Topoisomerase IIA enzymes (above) help to “unwind” DNA. During unwinding, while one part of the DNA strand unwinds, other parts would become tighter and tighter, and tangle unless cut and reconnected periodically during the unwinding operation. This is a good 2-minute video on the function of Topoisomerase:
Above is a diagram of the topoisomerase Type IIA enzyme. The red and blue domains are identical and are coded from the same gene, but they have to connect to each other to make a workable unit.
Note how the two identical copies nicely dock with each other to make a working machine. It is not a trivial task to design the right sequence of amino acids such that two topoisomerase polypeptides make the right fold in the first place. But they also have to create locations where the copies can connect to each other in order to form a working machine (a homodimer), as in the diagram.
The really amazing thing is that not only do the two identical pieces connect to each other to make a working unit, they act as moving parts in a process that accomplishes the following:
Detect and locate DNA that needs to be untangled (in order to relieve topological strain)
Cut the DNA using energy from ATP (an ATP site is provided on the topoisomerase)
Untangle the DNA after cutting
Re-connect the DNA strands where it was cut
The size and shape of the complex is important so as to accomplish its task on the size and shape of DNA.
Though there might be simpler genomes that don’t need topoisomerase, it is an important step for management of larger genomes. Topoisomerase is a target of chemotherapies because it is so life critical to cells.
In light of this and the criticality of its function and the criticality of each of the steps it follows in its enzymatic role, it is not probable that it evolves in gradual steps. This did not prevent evolutionary biologists from putting forward their usual phylogenetic “reconsctructions” that totally avoided the problem of lethal intermediates, but pretended to solve the evolution of topoisomerases.
The nice thing is that the Intelligent Designer decomposed the design into somewhat manageable discrete components like Proteins. We can climb the stairway of understanding from major elements of life (Hydrogen, Oxygen, Carbon, Nitrogen, Sulfur, Phosphorous) to monomers, to macro molecules made of monomers. But it is clear from Tan and Stadler’s work, the levels of organization don’t evolve naturally from pre-biotic mixtures because of problems like half-lives of the biomolecules and the asphalt paradox.
Just because the problem is CONCEPTUALLY decomposable into small steps, it does NOT imply it is can be physically evolved one step at a time, in fact the more we learn, the more it doesn’t seem to be naturally evolvable in systems like Topoisomerase.
The evolution of crystallins (the primary protein of the camera eye lens) is a classic example of repurposing genes to radically different ends:
This is nothing more than “I can’t come up with a story for how that evolved, therefore it didn’t, and God must have done it”. You can dress it up with pretty pictures, but that’s what you have. Most people don’t consider that a valid form of argument.
And I ask again: why do you pick fiat creation over divinely assisted evolution?
How about this, and that, and the game of whack-a-mole, and moving goalposts? It’s the if-you-don’t-know-everything-you-don’t-know-anything fallacy. We can (and do)have entirely rational grounds for concluding that extant biodiversity and it’s genetic and physiological characteristics are the product of evolution without having to explain literally everything down to the last molecule.
No, it’s been comprehensively answered. Changes in the regulation of genes which affect the absorption and scattering of light hitting the cell is how cell transparency can evolve either up or down.
Which naturally lend themselves to incremental mutational change, affecting how they function, encoded in a system of genetic molecular polymers which also naturally lend themselves to incremental mutational change. Heck, we even know of all the types of mutations that are possible, which are basically all the change, copy, insert, and rearrangement-tools one could imagine would be necessary for the function for an incrementally changing system of polymer sequences.
It’s almost like genetics is exactly the kind of thing that enables and facilitates the slow gradual process of evolution, whereby in splitting populations of organisms, the independent accumulation of genetic mutations with their changing effects on phenotype are subject to natural selection.
Thank you for the references.
However, change in cell-type is repurposing a lot of pre-existing material as well.
I’ll look at your references. And again, thanks you for the papers that you provided on the Stairway to Life thread that had table 3 that showed non-biological means of creating ATP.
I think a lot of protein families are multi-purpose (not re-purposed). That is clear from the nested hierarchies that exist for major protein families.
Evolutionary biologists interpret this nested hierarchy as evidence of common descent, but I think that is mis-interpretation as illustrated by the problem of necessary paralogs needed for Microtubule polarity.
In humans, it has been experimentally confimred the Topoisomerase paralogs are also necessary as well as paralogs of collagen. If paralogs are simultaneously necessary for functioning organisms, it stands to reason the nested hierarchy is not necessarily the product of natural common descent.
Nevertheless, thank you for the papers.
To my knowledge all opsins ultimately derive from pre existing and even older GPC receptors involved in detecting and responding to chemicals detected in the environment. If that’s not olfactory reception, or a sense of smell and taste, what else would you call it?
I’m just reporting the what needs to change, the lentis retractor muscle (in some fish) to the ciliary muscles (in humans). This also involves changes in neurons and coordination. Obviously you and Dr. Harshman think this is a sufficiently easy transition, but I (and I expect some of the readers of the books project) to consider it absurd.
I KNOW from experience that when I start describing things like this in detail, people are inspired with wonder at the Creator and how insufficiently Darwinisim (and/or even neutral theory) are as explanations. I point out, fossils like the fishapod don’t explain the sort of fine transitions that are actually needed to convert a fish to a human. I point out the absurdity of suggesting that this fossil
is good reason to believe the lentis retractor muscle in some fish can evolve into a ciliary muscle in humans.
Phylognetic reconstructions and nested hierarchies are not adequate to explain the issue of mechanistic feasibility of the numerous examples listed in this thread.
Many proteins like Zinc Fingers have specific binding targets on the genome at fine-tuned levels of binding affinity.
I demonstrated elsewhere the absurdity of nested hierarchical reasoning as some sort of mechanistic explanation for the evolution of Zinc Finger arrays:
The spelling of individual zinc fingers must be coordinated to bind with the right specificity and affinity to precise segments on the genome, otherwise the protein fails to funciton, and worse binds to the wrong places!
Appealing to hierarchical diagrams as some sort of explanation for how the zinc finger array matches the DNA is an absurd non sequitur.
Pointing out the non-sequitur of nested-hierarchy-type “explanations” in the above example is extensible to supposed zinc finger protein evolution between organisms, and really to nested-hierarchy explanations in general. The nested-hierarchies EXIST, but it is a non-sequitur to argue they are descriptions of the mechanical feasibility of evolving one thing to another – they are not because it takes more to make a protein functional in a functional context than just randomly evolving it. The KRAB Zinc Finger family proteins are an example.
Paralogs often evolve to specialise functions, yes. And? You’re conflating modern paralogs being necessary for modern organisms with modern paralogs being necessary for all organisms. Why do you find it the least bit surprising that paralogs evolve important functions? Make a change, then make it necessary. It’s not rocket science.
That’s new to me. Is there a review or something you could point to?
I would be happy to provide some feedback from the perspective of a well-informed amateur. I’m not a degree-holder, but I’ve read a lot of discussions and not-a-few papers. Most importantly, over the past two decades I’ve gone from the school of:
“Wow! These changes are huge and amazing! No way they could be produced by evolution!”
To the school of:
“Wow! These changes are huge and amazing! And even more amazing is that biologists, created in God’s image, are thinking God’s thoughts after Him; they have identified mechanisms by which the huge, amazing changes happen!”
The Unsuitability of the Staircase Metaphor
In this thread biologists have identified a fundamental problem that you have never addressed: the suitability of the staircase metaphor.
The problem is that evolution does not really follow a staircase to complexity. Archaea first showed up 3bya, and they are still hanging around today. IIRC they are far more diverse and numerous than any other kingdom that emerged later. To paraphrase Etta James:
This is a man’s world, this is a man’s world
But it wouldn’t, it wouldn’t be nothing
Nothing without archaea or protozoa
We humans rely on symbiosis with thousands of species of prokaryotes. They are not in your field of vision because you have chosen an unfortunate metaphor–staircase–that is basically inaccurate.
The way you are tying the image of God to evolutionary outcomes is unsustainable. Yes, every human alive is created in God’s image! But the evidence for our divine imprint does not lie in natural history.
Appeal to Intuition
Secondly, you keep appealing to the large changes and implying that the size makes them so improbable as to be unreachable by evolution. Yet you are not presenting any statistical methodology; it’s an entirely an appeal to intuition.
Biologists have documented the power of neutral evolution and mutations in the regulatory gene network to produce huge, amazing changes. So when someone points out yet another huge, amazing change that occurred at some point, of course their prior is to think that it happened through neutral evolution and mutations in the regulatory gene network. That prior is what lies behind all the responses you have seen in this thread.
Moreover, biologists have strong evidence of negative selection to preserve delicate structures that have become essential for the survival of a living population.
Behind every post you have made in this thread is a negation of the biologists’ priors. Frankly, I don’t see that you have done the very hard work that would be necessary to disprove those priors. You are just saying “Huge! Amazing!” and choosing a different path.
You are allowed to choose a non-scientific path, of course. If you’re going to do that, though, you would do well to be candid about your method and acknowledge that it is the choice you are making.
The spiritual value of non-intuitive science
Ever since I learned about quantum mechanics, I stopped thinking that my intuition was of any help in evaluating the plausibility of a scientific theory. Evolution is another scientific discipline, like quantum mechanics, where stochastic, non-intuitive processes yield incredible results. The faithful in Christ who believe that all truth is God’s truth would do well to recognize the incompatibility of intuition and the stochastic branches of science.
In fact, there is a spiritual value to be gained from that incompatibility. If our intuition is unsuitable for understanding science, our intuition is probably not fully capable of understanding God, wouldn’t you think? The inadequacies of our intuition point to our need for God’s special revelation through the covenants, the incarnation, and the Scriptures.
I hope you–and maybe even your readers?–will find these thoughts helpful.
I’ll try to dig something up. Meanwhile there’s this: Opsin evolution: orgins of opsins - genomewiki
Opsins are definitely not the ‘original’ GPCR because these were already widely deployed at much earlier divergence nodes – yeast, protozoa, choanflagellates, trichoplax have GPCR but lack opsins. Nor are opsins the prototype for the ‘rhodopsin class’ R of the GRAFS classification of GPCR which again was established far earlier. Indeed, even the Ralpha subgroup with of rhodopsin class GPCR was well-established prior to the first metazoan opsin.
Opsins are thus latecomers, not pioneers, to a rapidly expanding paralogous gene clade within already full-featured GPCR. Judging by their closest extant blastp relatives among tens of thousands of GPCR at GenBank, opsins specifically arose as a gene duplication within the peptide receptor subgroup PEP. Indeed, certain of these proteins list opsins among their top ten best back-blast matches (ie have better matches than to almost all non-opsin GPCR). Note here that blast scores can be misleading because the ‘floor’ of percent identity is about 25% just due to universal conserved residues plus accidental matches.
It appears I must eat my own words, as I can’t seem to find any specific references that suggest opsins derive specifically from GPC receptors classified as olfactory receptors(in fact I found a reference that explicitly stated the diametrically opposite)*. And I can’t remember where exactly I got this idea from, so I suppose it could just be a false memory and I’ve got something mixed up.
Rather the evidence appears to suggest they’re more closely related to hormone and peptide binding GPC receptors that could just as well have functioned in cell-cell signaling within a multicellular organism. This is also discussed further down in the link I gave.
*They write: The evolution of opsin genes is in sharp contrast to that of OR genes. Opsin genes also belong to the rhodopsin-like GPCR superfamily, and thus they are distant relatives of OR genes. Homologous opsin genes can be identified in vertebrates, insects and other invertebrates, however, indicating that the origin of the opsin gene family is much more ancient than that of the OR gene family.
Could you explain what that colorful figure means?