Behe's response to Lenski's first post

[Edgar_Tamarian]

Male mice heterozygous for a null apolipoprotein B allele ( Apo B+/− ), a structural component of several classes of lipoproteins (chylomicron, VLDL, IDL, LDL), have reduced fertility associated with a decreased cholesterol plasma level. 1995 The urogenital tract appears normal, but the sperm count is mildly reduced, motility is decreased, and spermatozoa are unable to fertilize an oocyte in the presence of its zona pellucida 1996 The authors only evoked the hypothesis of an unknown role of ApoB in spermatogenesis. However, today the importance of epididymal maturation is well demonstrated for the acquisition of mobility and zona pellucida recognition, and ApoB is also expressed in the epididymis. Defects could thus come from posttesticular events . Since this work, the authors have not pursued their investigation on this model

Posttesticular sperm maturation, infertility, and hypercholesterolemia

[swamidass (S. Joshua Swamidass)]

@Edgar_Tamarian we have a much easier claim to defend: we aren’t sure, but it looks like a gain of function. Behe is defending a much more confident claim: we can very certain it was loss of function.

[Edgar_Tamarian]

@swamidass

we have a much easier claim to defend: we aren’t sure, but it looks like a gain of function.

There is no positive reason to think that way,

There is at least 2 positive reason to think otherwise.

1. Positive reason to think otherwise

For mice, having only half as much APOB activity protects them from a high fat diet. For polar bears, having mutated APOB genes protects them from a high fat diet. If the polar bear mutations acted to lower the activity of its own APOB, a result similar to that for the mouse might be expected.

2. Positive reason to think otherwise A computer program that analyzes mutations predicted APOB gene to be damaged.

In the absence of positive evidence to doubt a prediction made by PolyPhen-2 for this specific case, the results of the computer program should be taken into consideration to test experimentally

[swamidass (S. Joshua Swamidass)]

@Edgar_Tamarian

we have a much easier claim to defend: we aren’t sure, but it looks like a gain of function.

There is no positive reason to think that way,

Yes you are stubborn in ignoring all the positive evidence we have offered. I agree.

@Edgar_Tamarian

2. Positive reason to think otherwise A computer program that analyzes mutations predicted APOB gene to be damaged.

Totall falsehood.

[Edgar_Tamarian]

@swamidass

all the positive evidence we have offered

The only positive evidence that you could attribute to is the effective clearance of cholesterol from the blood, which itself could be explained not by the gain of function, but the loss of function.as with mice studies. However, there is also a second positive evidence-the prediction made by PolyPhen which forces us to conclude that it was very certain a loss of function.
Having said that, I opt for experimental verification.

[swamidass (S. Joshua Swamidass)]

Then you disagree with Behe then. Nice.

[Edgar_Tamarian]

I do not think Behe against experimental verification.

[NLENTS (Nathan H. Lents)]

@swamidass

Two papers were published in Protein Science. They were later retracted. I am not sure they should have been retracted.

Really??? Can you link to those? Why were they retracted?

[evograd (Blogging Graduate Student)]

@Edgar_Tamarian

However, there is also a second positive evidence -the prediction made by PolyPhen which forces us to conclude that it was very certain a loss of function.

Hasn’t this been explained to you already? PolyPhen cannot predict whether a particular mutation is loss- or -gain-of-function.

[cwhenderson (Curtis Henderson)]

@evograd

Hasn’t this been explained to you already?

It has been explained - I’ve seen this explanation multiple times and I’m barely perusing the thread. I don’t know why this keeps popping up.

[swamidass (S. Joshua Swamidass)]

@Edgar_Tamarian

I do not think Behe against experimental verification.

He does not “opt” for verification. He just made a conclusion, with only part of the data (the part he likes) and moved on.

I’m glad to see @mercer is rubbing off on you. It is good to disagree with Behe on this one, just as you are doing right now.

[NLENTS (Nathan H. Lents)]

Because when someone really wants to believe something, they will ignore all evidence to the contrary. That’s basically the whole reason ID exists at all.

[T_aquaticus]

@Edgar_Tamarian

Science is not only about making experiments but also generating scientific ideas , which could later be confirmed by experiments ․

Intelligent Design and creationism have failed at this task as well.

If you think I am wrong, you could describe the experiments we could run to test ID and creationism. Mind you, these can’t be tests of evolution. They need to be tests of ID/creationism.

@Edgar_Tamarian

But my point is this, if a scientist proposes a scientific idea, you should not jump and say false idea, you are a heretic, just because of your philosophical predisposition. Proposed scientific ideas should be respected if they are theoretically well grounded.

We can criticize those ideas if they fail to produce testable hypotheses.