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Nature Paper Reaches "Edge of Evolution" and Finds Darwinian Processes Lacking (Behe right again!)
Evolution News & Views ^ | October 6, 2009 | Michael Behe, Ph.D.

Posted on 10/07/2009 5:05:03 PM PDT by GodGunsGuts

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To: Wacka; GodGunsGuts
this paper shows that in this case, you can’t go back to the earlier form by just making a single mutation.

No, I think that the letter states that unless the 5 specific restrictive mutations are reversed a non-functional protein is produced when other "key function switching" mutations are reversed. IOW there is a definite order of mutations. Thus even with selection for the old function the protein will not evolve the old function, "You can't get there from here."

A ---> B is allowed.

B ---> A is not allowed.

21 posted on 10/07/2009 7:59:43 PM PDT by AndrewC
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To: GodGunsGuts

Interesting little tidbit abotu Joe Thornton’s claim that nature could ‘construct irreducible complexity’

“And these are the words that disappeared (in brackets):

Our goal is to illustrate how a complex, tightly integrated molecular system - [one which appears to be irreducibly complex] - evolved by Darwinian processes hundreds of millions of years ago....”

“Two days ago, I pointed out that it’s a tad inconsistent to say there is no scientific controversy about ID, when one is participating in that very controversy (as Thornton and in fact a whole lot of other scientists and scholars are). Seems Thornton didn’t like me calling attention to this. So goodbye to the phrase “irreducible complexity” from his University of Oregon webpage see: http://www.uoregon.edu/~joet/ the last sentence of the second paragraph

http://www.idthefuture.com/2006/04/say_it_aint_so_joe_thornton_pu.html

And here’s the link where Joe Thorton was refuted by Behe

“The Lamest Attempt Yet to Answer the Challenge Irreducible Complexity Poses for Darwinian Evolution”

“In tomorrow’’s issue of Science, researchers Jamie Bridgham, Sean Carroll and Joe Thornton of the University of Oregon claim to have shown how an irreducibly complex system might have arisen by a process they call “molecular exploitation.” Their paper, “Evolution of Hormone-Receptor Complexity by Molecular Exploitation,” Science 312 (7 Apr 2006):97-101 and an accompanying commentary by Chris Adami are sure to stir lively discussion. Mike Behe has already weighed in, [Here: http://www.idthefuture.com/2006/04/the_lamest_attempt_yet_to_answ.html] arguing that Bridgham et. al. haven’t even come close to answering the challenge of irreducible complexity. Tomorrow we’ll provide a detailed scientific response to the paper as well.”


22 posted on 10/07/2009 8:29:12 PM PDT by CottShop (Scientific belief does not constitute scientific evidence, nor does it convey scientific knowledge)
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To: GodGunsGuts

Here’s the truth about Joe Thornton’s supposed creation of IC (Which by the way doesn’t even begin to resemble IC in the slightest- no wonder he took down his original claim from his website- He obviously knew how lame his attempt was to show IC ‘could arise naturally’ given his lame examples)

“The study by Bridgham et al (2006) published in the April 7 issue of Science is the lamest attempt yet — and perhaps the lamest attempt that’s even possible — to deflect the problem that irreducible complexity poses for Darwinism.

The bottom line of the study is this: the authors started with a protein which already had the ability to strongly interact with three kinds of steroid hormones (aldosterone, cortisol, and “DOC” [11-deoxycorticosterone]). After introducing several simple mutations the protein interacted much more weakly with all of those steroids. In other words, a pre-existing ability was decreased.

That’s it! The fact that this extremely modest and substantially irrelevant study is ballyhooed with press releases, a commentary in Science by Christoph Adami, and forthcoming stories in the mainstream media, demonstrates the great anxiety some folks feel about intelligent design.

In the study the authors wished to see if two related modern proteins called the glucocorticoid (GR) receptor and mineralocorticoid receptor (MR) could be derived from a common ancestral protein. Using clever analysis the authors made a protein that they thought represented the ancestral protein. That protein binds several, structurally-similar hormones, as does modern MR. They then introduced two amino acid changes into the protein which are found in modern GR. The two changes caused the ancestral protein to bind the different kinds of hormones anywhere from ten- to a thousand-fold more weakly. That protein bound aldosterone about three-fold more weakly than cortisol. The authors note that modern GR (in tetrapods) also binds aldosterone more weakly than cortisol. So perhaps, the thinking goes, an ancestral gene that could bind both hormones duplicated in the past, one copy accumulated those two mutations to become the modern GR, and the other copy became modern MR.

Here are number of comments in response:

1) This continues the venerable Darwinian tradition of making grandiose claims based on piddling results. There is nothing in the paper that an ID proponent would think was beyond random mutation and natural selection. In other words, it is a straw man.

2) The authors (including Christoph Adami in his commentary) are conveniently defining “irreducible complexity” way, way down. I certainly would not classify their system as IC. The IC systems I discussed in Darwin’s Black Box contain multiple, active protein factors. Their “system”, on the other hand, consists of just a single protein and its ligand. Although in nature the receptor and ligand are part of a larger system that does have a biological function, the piece of that larger system they pick out does not do anything by itself. In other words, the isolated components they work on are not irreducibly complex.

3) In the experiment just two amino acid residues were changed! No new components were added, no old components were taken away.

4) Nothing new was produced in the experiment; rather, the pre-existing ability of the protein to bind several molecules was simply weakened. The workers begin their experiments with a protein that can strongly bind several, structurally-very-similar steroids, and they end with a protein that at best binds some of the steroids ten-fold more weakly. (Figure 4C)

5) Such results are not different from the development of antibiotic resistance, where single amino acid changes can cause the binding of a toxin to a particular protein to decrease (for example, warfarin resistance in rats, and resistance to various AIDS drugs). Intelligent design proponents happily agree that such tiny changes can be accomplished by random mutation and natural selection.

6) In the “least promising” intermediate (L111Q) the protein has essentially lost its ability to bind any steroid. In the “most promising” intermediate protein (the one that has just the S106P alteration) the protein has lost about 99% of its ability to bind DOC and cortisol, and lost about 99.9% of its ability to bind aldosterone. (Figure 4C)

7) Although the authors imply (and Adami claims directly) that the mutated protein is specific for cortisol, in fact it also binds aldosterone with about half of the affinity. (Compare the red and green curves in the lower right hand graph of Figure 4C.) What’s more, there actually is a much larger difference (about thirty-fold) in binding affinity for aldosterone and cortisol with the beginning, ancestral protein than for the final, mutated protein (about two-fold). So the protein’s ability to discriminate between the two ligands has decreased by ten-fold.

8) One would think that the hundred-fold decrease in the ability to bind a steroid would at least initially be a very detrimental change that would be weeded out by natural selection. The authors do not test for that; they simply assume it wouldn’t be a problem, or that the problem could somehow be easily overcome. Nor do they test their speculation that DOC could somehow act as an intermediate ligand. In other words, in typical Darwinian fashion the authors pass over with their imaginations what in reality would very likely be serious biological difficulties.

9) The fact that such very modest results are ballyhooed owes more, I strongly suspect, to the antipathy that many scientists feel toward ID than to the intrinsic value of the experiment itself.

10) In conclusion, the results (and even the imagined-but-problematic scenario) are well within what an ID proponent already would think Darwinian processes could do, so they won’t affect our evaluation of the science. But it’s nice to know that Science magazine is thinking about us!

http://www.idthefuture.com/2006/04/the_lamest_attempt_yet_to_answ.html


23 posted on 10/07/2009 8:35:16 PM PDT by CottShop (Scientific belief does not constitute scientific evidence, nor does it convey scientific knowledge)
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To: GodGunsGuts

Thanks for the ping!


24 posted on 10/07/2009 8:59:39 PM PDT by Alamo-Girl
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To: Moonman62; CottShop

See the following re: Joe Thornton. Hat tip to Cottshop for digging this up!

http://www.freerepublic.com/focus/f-news/2357164/posts?page=23#23


25 posted on 10/08/2009 9:37:02 AM PDT by GodGunsGuts
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To: scripter

Behe is one of two things:

Ignorant or a perjurer.

He stared in the Dover trial that there is no scientific evidence for molecular evolutio, There are tons of journals with articles on it.

He is either stupid or lied under oath.


26 posted on 10/08/2009 11:21:23 AM PDT by Wacka
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