A Scholarly discussion of ApoB

[Art (Arthur Hunt)]

@BenKissling

… 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.

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.

[Mercer (John Mercer)]

@BenKissling

I quickly ceasing to care what you mean.

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!

[swamidass (S. Joshua Swamidass)]

@BenKissling

I have wanted Behe to respond to Hunt’s stuff on tURF-13 ever since I first read it years ago.

I agree. We are waiting for him to respond. Why do you think he continues to avoid responding to it?

[NLENTS (Nathan H. Lents)]

You spelled my username wrong, that’s why I didn’t get notified of your response.

@BenKissling

But I will say for myself that I think tURF-13 does look designed to me.

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.

[T_aquaticus]

@BenKissling

I see. ApoB seems to have a very complex mechanism. What sorts of effects would you expect a degradative mutation to have? Hyper or hypocholesterolemia aren’t the only ways to degrade such a complex mechanism. Is that all you meant?

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.

[T_aquaticus]

@BenKissling

Interesting. How many of them are degradative, neutral and constructive? Or maybe how many would you predict are in those categories?

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.

[Rumraket (Mikkel R.)]

@BenKissling

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.

So, mutations subject to natural selection then.

[BenKissling (YEC/ID)]

@NLENTS

Hunt is claiming tURF-13 fits our design criteria. It isn’t my cognitive bias.

[BenKissling (YEC/ID)]

@T_aquaticus

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.

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.

@T_aquaticus

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.

So is that a prediction that 5-15 are constructive and beneficial or are you not answering the question again?

[BenKissling (YEC/ID)]

@swamidass

I agree. We are waiting for him to respond. Why do you think he continues to avoid responding to it?

I don’t know. What I do know is that proteins must form folds to have biological function in real cellular environments. Lol.

[T_aquaticus]

@BenKissling

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.

Do you have something besides speculation?

@BenKissling

So is that a prediction that 5-15 are constructive and beneficial or are you not answering the question again?

I thought that was an answer. Is there something specific you would like me to explain further?

[NLENTS (Nathan H. Lents)]

@BenKissling

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,

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.