Thanks, as always, for this thoughtful reply, Nathan. As one whose attitude and understanding has been greatly affected by the dialog here (at PS over time), I really appreciate what you are saying. I came to PS because I wanted to see if there wasn’t some sort of unified theory of how things got here, what degree of agreement exists, and how such a philosophy might be articulated to the laypeople who are interested in this topic.
Many of us can envision the hand of God being involved in some way regarding the structure of the cosmos, the origin of life, and its evolution over time. If and how that happened may never be known for certain. But when we have a voice which carries authority (such as yours or Joshua’s) that merely leaves open the possibility of God’s involvement, it keeps open the door for a peaceful dialog, and also the minds to develop a greater understanding of the work that you in the science community are engaged in.
The door on God’s involvement is as open as the door on leprechauns, Muad’Dib, fairies, Santa Clause, Gandalf, the flying spaghetti monster, and Obi-Wan Kenobi.
I have wanted Behe to respond to Hunt’s stuff on tURF-13 ever since I first read it years ago. But I will say for myself that I think tURF-13 does look designed to me. That does not mean I think God miraculously causes those mutations directly. What I would hypothesize is tURF-13 is the result of what James Shapiro calls natural genetic engineering. In other words I would predict a mechanism similar to the immune system that mixes and matches genetic modules until it gets something that solves the problem was involved. This is in principle a testable prediction, and that is a valid scientific approach.
That’s not what we mean by a testable hypothesis. The prediction must be empirical–that is, what you will directly observe, with no wiggle room for interpretation.
So, @Rumraket, are you saying that you can, from science, know for certain that God was not involved at all? Leaving out the leprechauns, etc., for now at least. This seems to fly in the face of what Nathan said.
No, I can’t know that for certain. That doesn’t mean there are any good reason to even entertain the idea any more than the rest of the options I listed. There’s an infinite list of conceivable dial-twichers hiding behind the scenes. I could be causing these mutations with my telekinetic powers too, can you really know for certain that I’m not?
No, I cannot. Not from science anyhow. From the perspective of science, it is equally likely that you and Obi-Wan possibly are in cahoots with one another. It may be less likely for the leprechauns and Santa, however.
The point that I was trying to make is that it is refreshing to read a conversation over science that does not overstep its bounds and, as such, become exclusive to many groups of people. And, if you happened to be flipping the switches… well that’s a nice bit of work! Kudos!
We know how the gene came about, and it did not involve processes or sequences that come even close to fitting the bill of what Shapiro calls natural genetic engineering. Unless Shapiro wants to co-opt all recombination events, including the many many events involving sequences that have nothing to do with protein coding or even gene coding, into his models. Which would make his ideas no different from random mutation.
Of course! I’m just a geneticist and a biochemist who studies the effects of pathogenic mutations on structure and function. That’s way too relevant to your wishful thinking!
You spelled my username wrong, that’s why I didn’t get notified of your response.
I don’t mean this as harshly as it may sound, but that is your cognitive bias talking. If you want to see it that way, you’ll see design everywhere. That was the dominant view for thousands of years and it didn’t yield to scientific explanations quickly or easily.
If ApoB is not performing its function of transferring dietary lipids to the blood stream or clearing cholesterol from the blood stream then I would expect hypo or hypercholesterolemia.
It’s hard to say since a lot of these are extremely rare mutations. I also looked at allele frequency and there appeared to be 10 to 20 alleles that are found at >1% with the known 5 or so disease alleles among them. Overall, I would expect the majority to be neutral mutations.
Well obviously. What I meant was it seems to me ApoB has a very complex mechanism with several functions. There could be a number of them which are messed up by these mutations, some of which might not cause either hyper or hypo. For instance, suppose it’s getting targeted by ubiquitin for degradation is degraded. Or suppose some signaling or splicing sequence somewhere is degraded. All of these might affect its expression in ways that cause slight changes to metabolism or even to something completely unrelated, such as ubiquitin being freed up to target other proteins for example.
So is that a prediction that 5-15 are constructive and beneficial or are you not answering the question again?
That’s a lot of speculation there, with no evidence that specifically supports any of it. Do you consider those possibilities more likely than the explanation that does have evidence supporting it? (That explanation being that polar bear APOB has context-specific enhancements in cholesterol clearance via mutations in the relevant domain followed by natural selection) If you prefer unsupported speculation over a supported and uncontroversial hypothesis, you just might have some cognitive bias.