No, I’m seeing that Axe was responding to a request for comments on his 2004 paper: “In August of 2004 I received an email inquiry from plant biologist Art Hunt. He had written a draft for a blog piece aimed at reviewing a research article of mine that had just appeared in the Journal of Molecular Biology [1], and he wanted to know whether he had understood my work correctly. He clearly aimed to refute claims that were beginning to surface that my paper supported intelligent design, but he also wanted to make sure he wasn’t misconstruing my work in the process. He didn’t expect me to oblige—’I will understand if you decline; in fact, I would probably do the same…’—but I did.”
Then we read: “Here I summarize what appear to be the four most common objections to using my 2004 paper in support of ID, three of which trace back to Hunt’s blog entry, the fourth perhaps originating with Steve Matheson, who joined Art Hunt last summer for critical dialog with Steve Meyer in front of an audience at Biola University.”
So maybe you say this because you are thinking Axe was responding to your later article. Do please read what Axe said he was responding to, I presume you did send him a request for comments, and then address the reply he made.
As far as your 2007 article is concerned, glad to discuss that, too.
“Recall that Axe did not work with the native TEM-1 penicillinase, but rather with a variant that had a lower activity. The assay system made this necessary.”
Actually that’s not what Axe said about his choice, he describes why he made his choice of a variant with lower activity in his response, this therefore needs a response from you.
“In addition, Axe deliberately identified and chose for study a temperature sensitive variant. In altering the enzyme in this way, he molded a variant that would be exquisitely sensitive to mutation.”
Well, ditto, Axe explains why he did this, as mentioned above, and his counterpoint is what needs a response now.
You continue, “One of these, the metallo-beta-lactamases (Daiyasu et al., 2001), is quite unrelated to the TEM-1 enzymes. Axe’s study does not “count” these families of enzymes (or their neighbors), nor does it acknowledge that many more such structures are at least hypothetically possible.”
But I think it’s quite appropriate to pick one enzyme, and see how far away other functional enzymes might be. Why he needs to examine all possible enzymes that could have such a function is a mystery to me.
Then we have “To give the reader a sense of the higher end (10^-10) of this range, it helps to keep in mind that 1000 liters of a typical pond will likely contain some 10^12 bacterial cells of various sorts. If each cell gives rise to just one new protein-coding region or variant (by any of a number of processes) in the course of several thousands of generations, then the probability of occurrence of a function that occurs once in every 10^10 random sequences is going to be pretty nearly 1.”
But you don’t get a new variant in every cell. Your argument doesn’t work, if variants can be duplicates, which they can be.
Back to your post here!
But I don’t see this in your essay, which was just examined here. And I thought that Axe was sampling variants, to see how often functional variants occurred. Nothing about measuring parts of the bases of peaks.
I’ve been trying to diligently respond to objections in this thread, actually, thanks for your additional reply here. Glad to discuss this point in detail, why does Axe’s method not reliably distinguish between functional and non-functional variants?