Defining "complexity"

[Witchdoc]

@Giltil

If highly functional proteins are rare in sequence space, you are wrong on this matter. And I think a case can be made that highly functional proteins are indeed rare in sequence space.

Random sequences are an abundant source of bioactive RNAs or peptides

https://www.nature.com/articles/s41559-017-0127

Essentially all sites of a protein are mutable given other compensatory mutations

Sequence space and the ongoing expansion of the protein universe - PubMed

There are 1. 6 x 10^13 sequences of 35 amino acids that would fold like villin, and 7.9 x 10^96 171 amino acid sequences that fold like OmpA.

Gil grabs some ammunition and shoots down Doug Axe's 2004 extrapolation by a factor of more than 10^44

Continuing the discussion from Optima in Evolution: That’s fascinating, Gil, because you seem to have forgotten that less than 4 months ago you paid homage to Doug Axe: I’d say that they are not scholars and that they are irrational. Axe’s extrapolation, predictably misrepresented as fact by Meyer and many other ID creationists, was: “…this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10^77…” in the abstract, and “So, if set S is about one-thousandth the size of set H (as above), then the proportion of all sequences of large-domain length that perform the specified function by means of any tertiary fold (i.e. fall within the dark portion of F) is estimated to be in the range of one in 10^77 to one in 10^53.” in the discussion. Note that Axe’s colleagues AFAIK have never acknowledged the other bound Axe set and only cite 10^-77. So my question to you is how you reconcile the table you presented with …

If you want the original article, it is here

How Many Protein Sequences Fold to a Given Structure? A Coevolutionary Analysis

This high number actually poses a problem for creationists - if there are so many alternative sequences with the same function, with all amino acid sites mutable while retaining function, why do organisms’ DNA homology sort into clades, giving us evidence for common descent?

What is even more interesting that “complexity” is inversely proportional to age of the protein.

Optima in Evolution

So what? That doesn’t help you; it’s a sample. But since you’re taking this as gospel, what those numbers do to Doug Axe’s extrapolation? A design hypothesis would predict no correlation between the numbers of known proteins with each fold (folds do not correspond to functions) and the SC. In fact, the opposite is true, as the authors note that it is correlated with the size of a gene family. How do you explain that with a designer?

This is evidence that proteins of certain function start off smaller and less complex, then with time they evolve and become more complicated.

But hey, you should already know all this, given this was all presented to you previously here at peacefulscience.