Further mutations might make the interaction more essential and make the two subunits more dependent on one another. This is a perfectly reasonable scenario for the evolution of irreducible complexity. Anyone who claims that the very existence of irreducibly complexity means that a structure could not have evolved is wrong.
The claims of this paper are without substance. Where is the model that demonstrates this? You need to explain how DNA organizes in an innovative way. Two proteins somehow get dependent on each other and now you have a spliceosome with 80 or more proteins?
@swamidass I donāt think this should be endorsed until someone can show a plausible model and not just make a āthis could be possible statementā. There is no reason to believe a non deterministic mechanism can build a complex functional proteins structure where sequence comparison data shows high levels of preservation.
Another Bill evidence free assertion.
But they are not on their own. They are part of a biological organism. And maybe that organism can find an innovative way of using the genetic change.
You assert that the intelligent designer hypothesis predicts greater DNA similarity for greater design similarity. I disagree vigorously because there are a bazillion features in biology such as fish fins and dolphin fins that do not manifest the mathematical relationship. But I will accept it in arguendo for the moment.
What the intelligent designer hypothesis does not predict is any particular pattern for the statistical distribution of the nucleotide differences.
Evolution, on the other hand, predicts both the similarities and the statistical distribution of nucleotide differences.
When a scientific community has a choice between
(a) a vague model that predicts only one class of data, and
(b) a theory with with observed mechanisms and highly specific, mathematical predictions for several classes of dataā¦
Should it pick (a) or (b)?
Best,
Chris
I think the answer, Bill, is that some proteins are functional but their DNA instructions are not highly conserved. Thatās the evidence youāre missing, but the proponents of CNE are not.
As always, I welcome any corrections from those who has studied the literature deeply.
You have 100% misunderstood the point @swamidass was making.
Now that I have mentioned this to you, Iāll bet you can go back, re-read Dr. Swamidassā statement, and figure out its relevance to this thread.
Best,
Chris
Please. You expect me to believe you read that paper and all the accompanying papers in an hour? Tell us how itās without substance
Man, youāre a nice guy.
Have you even tried searching for that?
There are countless models, simulations, and actual experiments, that demonstrate the reality of the effect.
Hereās some recent article on modeling the evolution of protein interactions and folding:
Zabel WJ, Hagner KP, Livesey BJ, Marsh JA, Setayeshgar S, Lynch M, Higgs PG. Evolution of protein interfaces in multimers and fibrils. J Chem Phys. 2019 Jun 14;150(22):225102. DOI: 10.1063/1.5086042
Manhart M, Morozov AV. Protein folding and binding can emerge as evolutionary spandrels through structural coupling. Proc Natl Acad Sci U S A. 2015 Feb 10;112(6):1797-802. DOI:
10.1073/pnas.1415895112
Iām sure you can read those and explain how itās all without substance in about an hour. And continue to insist that it ācanāt be modeled?ā. āWhere are the models?ā āThere are no models!ā Etc. etc.
On the topic of CNE, what happens to begin with is two proteins stick together. And proteins in general can do that, they have an intrinsic tendency to aggregate. In fact this can be something of a problem as some proteins can form amyloids and cause various forms of disease.
However, some times this sticking together is neither helpful nor a hinderance, both proteins just carry out the function they do while sticking together. In such situations, it is likely that a functionally degenerative mutation in one protein will occur which makes it slightly worse at doing what it is doing if it is alone. But now the sticking together with another protein can compensate for this degenerative mutation. The same thing happens to the other protein, it suffers a mutation that degrades itās function while it is alone. Now the two proteins function worse if they are by themselves, but since they have a tendency to stick together, each of their presence compensates for this loss in both of them. Further degenerative mutations in each protein just increases this mutualistic relationship until, eventually, neither of them can perform their individual functions without the otherās presence. They have become completely dependent on the partner, the system has become irreducibly complex.
And hereās an article where the Thornton Lab demonstrates that this is how increased complexity evolved in the molecular machine ATP synthase:
Finnigan GC, Hanson-Smith V, Stevens TH, Thornton JW. Evolution of increased complexity in a molecular machine. Nature. 2012 Jan 9;481(7381):360-4. DOI:10.1038/nature10724
Abstract
Many cellular processes are carried out by molecular āmachinesā-assemblies of multiple differentiated proteins that physically interact to execute biological functions. Despite much speculation, strong evidence of the mechanisms by which these assemblies evolved is lacking. Here we use ancestral gene resurrection and manipulative genetic experiments to determine how the complexity of an essential molecular machineāthe hexameric transmembrane ring of the eukaryotic V-ATPase proton pumpāincreased hundreds of millions of years ago. We show that the ring of Fungi, which is composed of three paralogous proteins, evolved from a more ancient two-paralogue complex because of a gene duplication that was followed by loss in each daughter copy of specific interfaces by which it interacts with other ring proteins. These losses were complementary, so both copies became obligate components with restricted spatial roles in the complex. Reintroducing a single historical mutation from each paralogue lineage into the resurrected ancestral proteins is sufficient to recapitulate their asymmetric degeneration and trigger the requirement for the more elaborate three-component ring. Our experiments show that increased complexity in an essential molecular machine evolved because of simple, high-probability evolutionary processes, without the apparent evolution of novel functions. They point to a plausible mechanism for the evolution of complexity in other multi-paralogue protein complexes.
Nobody says ātwo proteins become dependent on each other and then POOF thereās a spliceosome with 80 or more proteinsā. Except Sal does. And you like that. So you have a hypocritical double standard.
I did not miss this:
āWe can do a similar comparison between species. Count up all of the fixed nucleotide differences between species and then calculate the spectrum of these types of differences, and then compare this to the spectrum of differences within just one of the species, or the spectrum from new mutations arising in one of the species species. The same logic applies as before. If mutations are responsible for the differences between species, then the spectra should match. If a process other than mutation is responsible, like divine creation, then thereās no reason to expect such a pattern.ā
Are you saying that since I am a creationist I am not allowed to believe in mutations and molecular change and the resulting differences between the two species?
Besides, wasnāt his paper also about āthe degree of similarityā (even though you say it was not), including similarity found in the differences?
We are talking about humans and chimps. Do you believe that humans and chimps share a common ancestor?
How? Educate me. How does line 2 force line 1 to fail?
Well, no. But that is beside the point right now. Question: are you suggesting that this study forces one to conclude divergence of proto humans and apes from a common stump? Are you declaring that there is no other way to explain the data?
Iām declaring no one has produced another mathematical explanation of the data. This is a fact.
Hmm. But now you are saying that the math here only belongs to and arises from common ancestry. I affirm the math too. So my question stands: is this data due only to a common stump between human/chimpanzee or is this data due to closely created kinds who had so much in common that it only looks like they share that stump?
We donāt know. But we do know that common descent gives us a mathematical explanation, while special creation does not.
And there the mystery. You must believe something about special creation that you are foisting on me. Because my view of special creation fully allows for the math. Educate me on the brand of special creation that you have in mind.
Produce the mathematical equations that explain these patterns then. Iām all ears.
Well the math looks very simple. Just plotting graphs. I could back into it but it will take some time. In the meantime, I must disagree with the authorās assertion here
" If a process other than mutation is responsible, like divine creation, then thereās no reason to expect such a pattern."
What I am saying is that I will back into the math, graph the very same thing as the author does, and we have gotten no further along in the argument, because I have no idea how special creation of humans and great apes confounds and eliminates the math.
Perhaps I will get some insight if this poster speaks up.