Another IDology challenge -- complete with complaints of harsh treatments ...

It is fabricated because it hasn't been empirically tested. It is a fabrication of the assumptions Axe makes.However, we can test Axe's calculations empirically. VDJ recombination during B-cell development produces billions B-cell lineages each with their own antibodies. The variable region of these antibodies can serve as a model for finding function. In fact, we can see if any of those antibodies have B-lactamase activity, the function that Axe says can only occur once in every 1x10^77 combinations.

quote:

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Here we report the construction of a large murine single chain fragment variable (scFv) phage display library of size 2.7 10^9 with extended diversity by combining different mouse models. We have used two molecularly different inhibitors of the RTEM lactamase as targets for selection of catalytic antibodies with lactamase activity. This novel methodology has led to the isolation of five antibody fragments, which are all capable of hydrolyzing the lactam ring.
Just a moment...

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In a library of 2 x 10^9 random peptides they were able to find 5 of those random peptides that had B-lactamase activity, well below the number given by Axe. Even if we look past all of the problems with Axe's mathematical model, reality shows us that Axe is wrong by many orders of magnitude.

The conclusions Axe drew from the results were faulty and fabricated. He assumed that his experiment would capture all possible B-lactamase proteins. If Axe's claim is not relevant to the chances of a functional B-lactamase emerging from random sequence, then his claim is irrelevant to evolution. Then what is it? So you are saying that it is easy to evolve a B-lactamase enzyme by randomly changing a small portion of the same protein? If so, then what is your problem with evolution?