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ORIGINAL: Jhud

Coincidentally, Michael Behe recently analyzed this paper here.

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This is not a coincidence.

Behe mentions The Edge of Evolution 4 times on his Amazon.com hosted "blog".

This is good marketing.

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ORIGINAL: Jhud

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This is not a coincidence.

Behe mentions The Edge of Evolution 4 times on his Amazon.com hosted "blog".

This is good marketing.

If you had read the book you would know why it's relevant.

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I have actually read the book, but it still doesn't make the "coincidence" not funny and self serving.
I've also read Darwin's Black Box.

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And so you would realize it isn't so 'coincidental' or self-serving after all.

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It certainly sounds like it; especially for an author.

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ORIGINAL: Jhud

Coincidentally, Michael Behe recently analyzed this paper here.

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Proc Natl Acad Sci U S A. 2008 Jun 4. [Epub ahead of print] Links
Inaugural Article: Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli.Blount ZD, Borland CZ, Lenski RE.
Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI 48824.

The role of historical contingency in evolution has been much debated, but rarely tested. Twelve initially identical populations of Escherichia coli were founded in 1988 to investigate this issue. They have since evolved in a glucose-limited medium that also contains citrate, which E. coli cannot use as a carbon source under oxic conditions. No population evolved the capacity to exploit citrate for >30,000 generations, although each population tested billions of mutations. A citrate-using (Cit(+)) variant finally evolved in one population by 31,500 generations, causing an increase in population size and diversity. The long-delayed and unique evolution of this function might indicate the involvement of some extremely rare mutation. Alternately, it may involve an ordinary mutation, but one whose physical occurrence or phenotypic expression is contingent on prior mutations in that population. We tested these hypotheses in experiments that "replayed" evolution from different points in that population's history. We observed no Cit(+) mutants among 8.4 x 10(12) ancestral cells, nor among 9 x 10(12) cells from 60 clones sampled in the first 15,000 generations. However, we observed a significantly greater tendency for later clones to evolve Cit(+), indicating that some potentiating mutation arose by 20,000 generations. This potentiating change increased the mutation rate to Cit(+) but did not cause generalized hypermutability. Thus, the evolution of this phenotype was contingent on the particular history of that population. More generally, we suggest that historical contingency is especially important when it facilitates the evolution of key innovations that are not easily evolved by gradual, cumulative selection.

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They don't state that this is due to two mutations, or even what the molecular mechanism is. Until that is determined the "Edge of Evolution" argument is without a mutation to work with.

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ORIGINAL: Jhud

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They don't state that this is due to two mutations, or even what the molecular mechanism is. Until that is determined the "Edge of Evolution" argument is without a mutation to work with.

Did you even read what Behe wrote?

He states that the mutations are currently unknown. But he makes a point about the type of mutations we can expect, and a prediction:

To get a feel for the clumsy ineffectiveness of random mutation and selection, consider that the workers in Lenski’s lab had routinely been growing E. coli all these years in a soup that contained a small amount of the sugar glucose (which they digest easily), plus about ten times as much citrate. Like so many cellular versions of Tantalus, for tens of thousands of generations trillions of cells were bathed in a solution with an abundance of food — citrate — that was just beyond their reach, outside the cell. Instead of using the unreachable food, however, the cells were condemned to starve after metabolizing the tiny bit of glucose in the medium — until an improbable series of mutations apparently occurred. As Lenski and co-workers observe: (Blount, Z.D., Borland, C.Z., and Lenski, R.E. 2008. Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli. Proc. Natl. Acad. Sci. U. S. A 105:7899-7906.)

Such a low rate suggests that the final mutation to Cit+ is not a point mutation but instead involves some rarer class of mutation or perhaps multiple mutations. The possibility of multiple mutations is especially relevant, given our evidence that the emergence of Cit+ colonies on MC plates involved events both during the growth of cultures before plating and during prolonged incubation on the plates.

In The Edge of Evolution I had argued that the extreme rarity of the development of chloroquine resistance in malaria was likely the result of the need for several mutations to occur before the trait appeared. Even though the evolutionary literature contains discussions of multiple mutations (5), Darwinian reviewers drew back in horror, acted as if I had blasphemed, and argued desperately that a series of single beneficial mutations certainly could do the trick. Now here we have Richard Lenski affirming that the evolution of some pretty simple cellular features likely requires multiple mutations.

If the development of many of the features of the cell required multiple mutations during the course of evolution, then the cell is beyond Darwinian explanation. I show in The Edge of Evolution that it is very reasonable to conclude they did.

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If the development of many of the features of the cell required multiple mutations during the course of evolution, then the cell is beyond Darwinian explanation.

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Isn't this exactly what your requirements are for proof of evolution? Multiple successive mutations working to form a new non-novel trait? This quote through and through makes it sound like he supports evolution, then at the last second... says it doesn't.

Each mutation itself doesn't have to be beneficial. It just has to be not harmful enough to survive in the gene pool.

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Perhaps you can clarify here.. I don't understand what he's getting at. His ideas on irreducible complexity rest upon the idea that it would be impossible for multiple successive mutations alone to form a new complex system. Now he's saying that multiple successive mutations possibly forming a new complex system are proof against evolution?

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ORIGINAL: Jhud

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Isn't this exactly what your requirements are for proof of evolution? Multiple successive mutations working to form a new non-novel trait? This quote through and through makes it sound like he supports evolution, then at the last second... says it doesn't.

Each mutation itself doesn't have to be beneficial. It just has to be not harmful enough to survive in the gene pool.

He doesn’t say anything about “Multiple successive mutations”, he says, “multiple mutations” – simultaneous mutations.

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Perhaps you can clarify here.. I don't understand what he's getting at. His ideas on irreducible complexity rest upon the idea that it would be impossible for multiple successive mutations alone to form a new complex system. Now he's saying that multiple successive mutations possibly forming a new complex system are proof against evolution?

Read a little more carefully – he says nothing about ‘successive’.

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Well, I think I picked that up from you. I don't feel like digging them up, but I seem to recall you saying something along those lines in the discussions over bat traits.

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ORIGINAL: Jhud
Behe: If the development of many of the features of the cell required multiple mutations during the course of evolution, then the cell is beyond Darwinian explanation. I show in The Edge of Evolution that it is very reasonable to conclude they did.

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In the case of citrate metabolism in E. coli it appears that there were at least two mutational events required only one of which produced cit+ colonies. What Behe claims Darwinian evolution can not do has been done in the lab. These were successive mutations given the fact that cit+ colonies formed more quickly if they went to a specific cit- generation.

However, we observed a significantly greater tendency for later clones to evolve Cit(+), indicating that some potentiating mutation arose by 20,000 generations. This potentiating change increased the mutation rate to Cit(+) but did not cause generalized hypermutability.

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ORIGINAL: Jhud

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In the case of citrate metabolism in E. coli it appears that there were at least two mutational events required only one of which produced cit+ colonies. What Behe claims Darwinian evolution can not do has been done in the lab. These were successive mutations given the fact that cit+ colonies formed more quickly if they went to a specific cit- generation.

However, we observed a significantly greater tendency for later clones to evolve Cit(+), indicating that some potentiating mutation arose by 20,000 generations. This potentiating change increased the mutation rate to Cit(+) but did not cause generalized hypermutability.

Interesting that you now do what you initially claimed Behe did - namely speak of what happened, even though, as you acknowledged, they don't even state, "what the molecular mechanism is".

Behe made a prediction - it won't be long before we know whether he was right or wrong.

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Even though the evolutionary literature contains discussions of multiple mutations (5), Darwinian reviewers drew back in horror, acted as if I had blasphemed, and argued desperately that a series of single beneficial mutations certainly could do the trick. Now here we have Richard Lenski affirming that the evolution of some pretty simple cellular features likely requires multiple mutations.

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So what is Behe saying here? That evolution can produce new traits through previously unselected mutations?

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ORIGINAL: Jhud
No, he is saying that in a few trillion individual organisms over the course of tens of thousands of generations, you occasionally get lucky and two mutations happen to correlate to allow for a simple beneficial ability - and even then, it is probably along the lines of over-expressing an extant gene.

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How many multiple residue functions evolved in these bacteria that were not selected for? Thousands? Millions? If they tested these bacteria against thousands of carbon sources at the same time they would have evolved to thousands of carbon sources in the same time period, would they not? The limiting factor here is not population, it's available niches.

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ORIGINAL: Jhud
No, the limiting factor is raw numbers and the chance of a particular combination of mutations occurring.

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And the availability of niches. Or are you saying that it was just chance that citrate metabolism is the only trait that evolved in these bacteria?

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ORIGINAL: Jhud
If the basis for such a trait is the two mutations, then that basis would be the product of chance and that chance would increase by the sheer number of organisms in existence.

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Read a little more carefully – he says nothing about ‘successive’.

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Well, I think I picked that up from you. I don't feel like digging them up, but I seem to recall you saying something along those lines in the discussions over bat traits.

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Well it is notable that these are two separate experiments dealing with two separate changes to the expression of two different genes. Even with those two changes one wouldn't have sufficient changes to make a 'wing', though the limb would certainly be more wing-like - so we can specifically and systematically explore what it would take – and if the evolutionists are right per the quoted scientists, then we should be able produce a series of 'successive slight modifications" each one representing a viable form - I am predicting this hasn't actually been the result, and will not end up being the result - and thus other factors are necessary, primarily organization and planning.