Stephen Meyer: “It is therefore overwhelmingly more likely than not that a random mutational search would have failed to produce even one new functional (information-rich) DNA sequence capable of coding for one new protein fold in the entire history of life on earth.”
Ahh the good ole bait and switch. Here Meyer is confusing the probability of randomly selecting a protein sequence adopting the beta-lactamase fold and catalyzing beta-lactam hydrolysis, with the probability of selecting a protein sequence able to carry out a fitness-improving function.
We are simply not required to believe that TEM-1 beta-lactamase was produced by de novo evolution from non-coding DNA. Incidentally we know from phylogenetic inference it evolved from DD-peptidases by duplication and divergence, not de novo from randomly picking stuff out of sequence space.
They always get this wrong, knowing it is wrong. @Agauger on this very forum has herself explained that Axe’s experiment is not an estimate of finding any novel functional protein in sequence space. It happened in this post
(My bold)
Ann Gauger: I don’t think you have understood Axe’s paper.That’s the most charitable I can be: you either don’t understand or are mischaracterizing. Your last sentence makes it clear. Axe estimates the prevalence of sequences that adopt a specific functional fold; he doesn’t expect every protein to be a beta lactamase. You must know that.
In his experimental case he used a particular beta lactamase and calculated the proportion of possible sequences with that fold that could carry out that function.
It becomes particularly interesting when we read what she says says next:
He then went on to generalize, making use of 2 studies with similar approaches, namely the use of mutagenesis to determine what proportion of sequences can carry out that fold’s function after mutagenesis.
That fold’s function. But the function of that fold can be carried out by protein with completely dissimilar folds. The function of beta-lactam hydrolysis. The break-down of beta-lactam antibiotics by consumption of water in the reaction. As noted Puck, the function has been selected in catalytic antibodies. It is known to exist in a completely different family of proteins known as metallo beta-lactamases which has an entirely different fold that is unrelated to TEM-1 beta-lactamase.
That means Axe’s experiment LOGICALLY cannot be an estimate of the “proportion of sequences can carry out that fold’s function!”, since that fold’s function exist in other folds. AXE 2004 IS TRASH.