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Author Topic:   The Death Knell for ID?
Trixie
Member (Idle past 2945 days)
Posts: 1011
From: Edinburgh
Joined: 01-03-2004


Message 1 of 102 (649988)
01-26-2012 3:40 PM


A new paper has not only cast doubts on Michael Behe's assertions, it's run a freight train over the top of the ID arguments against evolution.

For a concise version see

http://www.nytimes.com/...us-learns-a-new-way-to-infect.html

The abstract can be found at

http://www.sciencemag.org/content/335/6067/428.abstract

Science 27 January 2012: Vol. 335 no. 6067 pp. 428-432

I don't have access to the full text, so would appreciate the input of people who have.

Briefly, it has been shown that a bacteriophage which infects E.coli via the LamB receptor was able to evolve a different mechanism to infect E.coli cells which had very few LamB receptors on the surface. Within only fifteen days there were phage particles using the OmpF protein, something the phage had never been known to do before.

DNA analysis showed that 4 separate mutations were needed for the phage to use OmpF. Of 96 lines, 24 developed the ability to use OmpF and the mutations were identical or almost identical.

This is something that, according to ID, is so improbable that it would either never happen or would take far too long to happen by random mutation and natural selection. The probability of all four mutations occurring simultaneously is approximately 1 in a thousand trillion trillion, so it seems likely that they were gained one at a time, something ID and Behe dismiss out of hand. Even if we accept their claim that stepwise mutations can't result in something bordering on irreducible complexity, they are left dealing with the fact that something with such a low probability of happening, happened within 15 days!

I'd like a very open discussion on this and would like to include those who can't post in the science fora, but I would like the emphasis to remain on the science so have no idea where this would go, since moderation may be required. Whatever Admin decides is fine with me.


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Trixie
Member (Idle past 2945 days)
Posts: 1011
From: Edinburgh
Joined: 01-03-2004


Message 8 of 102 (650010)
01-27-2012 3:32 AM
Reply to: Message 6 by Portillo
01-27-2012 1:23 AM


Anything say on the sbstance of the paper?
The whole reason this paper is important is as follows

1. Behe and supporters of ID claim that this sort of thing can't happen, therefore ID is the only explanation.

2. It just happened in a lab in 15 days, not once, but many times.

Now either Behe is wrong and the foundation of the ID argument (they call it evidence) is fatally damaged

OR

The intelligent designer spent alot of time in the lab tinkering with the bacteriophages.


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Trixie
Member (Idle past 2945 days)
Posts: 1011
From: Edinburgh
Joined: 01-03-2004


Message 10 of 102 (650012)
01-27-2012 4:14 AM
Reply to: Message 4 by nwr
01-26-2012 10:52 PM


I agree that Dover should have put an end to the case for ID and I fully expected it to. However, Judge Jones showed much foresight when he said in the judgement that many would claim that it was a judgement of an activist court. Sure enough, this accusation is used time and again.

In the years since Dover, many bills have been introduced which show that ID is still trying to get a foot in the door by getting around the judgement using altered definitions and sleight of hand instead of dealing with the core finding of the judgement that ID isn't science. Behe's crucial claim, that certain things cannot happen by random mutation and natural selection, has been shown to be wrong, most notably in 2007 by Abie Smith (See Panda's Thumb and ERV's blog, I'll try to link later).

This paper in Science, however, is different, in that it doesn't compare isolates from 30 years ago to current isolates, but actually observed the "impossible" in real time, in an experiment, in a lab. Not only that, but it was observed happening multiple times. It seems to cover all the objections that ID followers put forward when confronted with this type of evidence.

Given that 4 mutations are involved in gaining the ability to use OmpF, it also makes inroads in the irreducible complexity argument, in real time, observed in a lab, again avoiding the criticism levelled at historical comparisons. This time the argument that "you weren't there to observe it so it's all guesswork" isn't going to work - the researchers were there, they did observe it and no guessing was involved.


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Trixie
Member (Idle past 2945 days)
Posts: 1011
From: Edinburgh
Joined: 01-03-2004


Message 11 of 102 (650013)
01-27-2012 4:27 AM
Reply to: Message 9 by Tangle
01-27-2012 4:06 AM


Intermediate selection
Hope this helps, please forgive the huge cut and paste, but it was the easiest way to provide this information.

Nonetheless,
there are several lines of evidence that selection
drove their rise. First, all 248 independent mutations
in the 51 sequenced J alleles were nonsynonymous,
whereas the expected ratio of nonsynonymous
to synonymous changes is 3.19:1 under
the null model for the ancestral J sequence (16).
This great excess is evident even if we include
only the 82 nonsynonymous mutations in the
24 isolates that did not evolve the new receptor
function. Second, the mutations are highly concentrated
in the region of the J protein that interacts
directly with LamB (18). Third, there was
parallel evolution at the genetic level across the
populations. For those phage that evolved to exploit
OmpF, an average of 61%(4.06 out of 6.63)
of mutations were shared across independently
derived pairs (fig. S7), which greatly exceeds the
fraction expected under a conservative randomization
test (16) that used only the variable sites in
J (P < 10−5). Pairs of phage that remained dependent
on LamB shared on average 17% (0.58
out of 3.42) of their mutations (fig. S7), and this
fraction is again significant under the same test
(P < 10−5). Thus, it is clear that selection acted
on the J protein even before the new capacity
evolved. This selection presumably improved the
interaction of the phage tail with LamB.

From the Meyer paper


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Trixie
Member (Idle past 2945 days)
Posts: 1011
From: Edinburgh
Joined: 01-03-2004


Message 16 of 102 (650032)
01-27-2012 7:02 AM
Reply to: Message 13 by Wounded King
01-27-2012 4:55 AM


Wounded King writes:

I would suggest that the fact that the intermediate forms seem to provide a selective advantage and the fact that the 4 mutations are not so highly specific are the most likely reasons an ID proponent might put forward for this not being a case that demonstrates the evolution of a truly irreducibly complex system, whatever one of those might really be.

They may put that forward, but the fact that the 4th mutation required for the utilisation of OmpF didn't occur without the previous 3 raises an interesting question. What would happen if one of those initial 3 was knocked out, so you had steps 1, 2 and 4 or 2, 3 and 4? Their data suggest that steps 1,2 and 3 are absolutely required for step 4 to take place, but once step 4 is in place, how necessary are the previous steps or can one or other then be discarded? The early mutation that increases the phage's affinity for the rare LamB binding site can possibly be knocked out now that the phage has an alternative, abundant binding site (although I'd like to see this shown experimentally). That also means that further mutations at that site may now be more "survivable"

I think this demonstrates the fault that Behe makes when he starts with a "completed" IR system and then tries to work back. Not every step that resulted in an IR system may still be hanging around. Rather than working backwards, it's more productive to try to work forwards. It's a bit like building something that requires scaffolding to be put up. Once the build is complete, the scaffolding is removed. An IDist would look at the building and suggest that the builders flew up to the higher levels to do the work, a scientist would suggest ladders, hoists and scaffolding to reach the higher levels. While not an ideal analogy, I can't come up with a better one. Feel free to suggest some as analogies are so useful in explaining things.


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Trixie
Member (Idle past 2945 days)
Posts: 1011
From: Edinburgh
Joined: 01-03-2004


Message 21 of 102 (650071)
01-27-2012 11:31 AM
Reply to: Message 18 by Wounded King
01-27-2012 8:30 AM


Wounded King writes:

I don't think the sort of strict sequentiality you seem to be describing here really exists.


Point taken. I was trying to keep things simple.

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Trixie
Member (Idle past 2945 days)
Posts: 1011
From: Edinburgh
Joined: 01-03-2004


Message 31 of 102 (650176)
01-28-2012 3:36 PM
Reply to: Message 30 by Percy
01-28-2012 1:54 PM


Re: Research Cited by the Biologic Institute
In a word, nope!

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Trixie
Member (Idle past 2945 days)
Posts: 1011
From: Edinburgh
Joined: 01-03-2004


(4)
Message 38 of 102 (650430)
01-31-2012 7:08 AM
Reply to: Message 35 by Robert Byers
01-31-2012 1:26 AM


Substance, please
This thread is about the implications of the recent publication which I mentioned in the opening post. If you don't wish to discuss these implications, or show where the paper is in error, then don't post, simples. Rhetoric doesn't cut it.

Why don't you give me some of the "fingerprints" which are "obvious and measurable" and the measurements of them which refute the paper in question? Tell us who measured them and by what means. After all, if they're measurable then someone must have measured them to try to show evidence for ID.

So can you provide this data, like the authors of the paper in question do? They don't just assert that they've done an experiment which gave results which gel with the ToE. They give their Materials and Methods, chapter and verse, their Results, chapter and verse and their Discussion of the results, chapter and verse and they do all this in public so everyone can see what they did and what they found. They're opening up their work to scrutiny, they have nothing to hide and anyone is free to comment on the substance of their work. What work has ID done this with?

If all you have are soundbites, rhetoric and unfounded assertions then your position is intellectually bankrupt and deserves the ridicule and criticism which has been heaped upon it, both in academia and the courts.


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Trixie
Member (Idle past 2945 days)
Posts: 1011
From: Edinburgh
Joined: 01-03-2004


Message 52 of 102 (652738)
02-15-2012 6:06 PM
Reply to: Message 51 by Genomicus
02-15-2012 5:51 PM


I think you've got it a bit back to front. When Behe witters on about irreducible complexity he specifically states that he rejects the idea of incremental improvements finally resulting in a complex change. It's been suggested by him that each step along the path to an "irreducibley complex" end result wouldn't happen because nearly all mutations are deleterious. This study shows how that is false. Once the final mutation is in place, the others can be lost and the phage will survive. However to get to the final mutation, prior mutatiojns to at least increase survival chances a little are required (increase in affinity of the phage J protein for LamB).

I'll respond in more detail if required tomorrow, I'm just in from the movies and very tired.


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Trixie
Member (Idle past 2945 days)
Posts: 1011
From: Edinburgh
Joined: 01-03-2004


Message 60 of 102 (652759)
02-15-2012 8:53 PM
Reply to: Message 59 by Wounded King
02-15-2012 7:47 PM


Re: Deja Vu
As far as I could tell, the fourth mutation never occurred without the others, but the others occurred without the fourth. Additionally, the ability to use OmpF was exclusively seen in those which had the fourth mutation so it was the fourth one which allowed the phage to utilise OmpF as an attachment point. The authors suggest (but don't have data to support this) that initially the other mutation(s) increased the affinity of the J protein in the phage tail for the very rare LamB receptor site on the E. coli.

Under normal circumstances bacteriophage lambda doesn't use OmpF, only LamB. When confronted with an E.coli host with down-regulatulation of LamB on the surface, those phage particles which gained a mutation which increased their chances of finding and binding to the much rarer LamB were more likely to survive. Without these the phage couldn't survive to achieve the final mutation which switched it's attachment point from LamB to OmpF. Once the bacteriophage had achieved this it no longer requires LamB to attach to the surface of E.coli, since most, if not all E.coli express OmpF on their surface.

If the bacterium subsequently loses the mutations which conferred the increased affinity for LamB, you'd be looking at a simple example of an "irreducibly complex" system, i.e., how, in the absence of it's only receptor, could the bacteriophage manage to evolve the final mutation, given that evolution requires the survival and replication of the phage and it can't do that if it can't infect the bacterial cells.

As an aside, a claim has been made that the team "deliberately" used a "weakened" strain of phage which reverted back to the stronger type in the first step. I've checked this out. The strain used was cI26 and the Supplementary Material supplied to Science along with the paper provides a table of mutations that this strain harbours, in comparison with the wild type. Using the wild type whole genome sequence fromGenbank I located the gene for the J tail fibre protein and none of the listed mutations occur within this gene. Having said this, it was someone on Centre for Intelligent Design, UK so it's not surprising that it was a completely erroneous suggestion.

Behe ran a computer simulation in the past to see how long it would take to acquire two previously specified mutations (Behe & Snoke, 2004). The parameters he set up included having no survival advantage on a single mutation. He got his 2 mutations after 20K (about 2 years) generations AFAIK. He spoke about this at Dover. His problem was that something he said couldn't happen, did happen. Not only that, but the numbers in his starting population didn't even represent the number of bacteria in 1 ton of soil. I calculated how quickly his two mutations would occur in 1 ton of soil and it came out at 0.7 days. His evidence in regard to his very own data was destroyed at Dover.

As for the resistance of the malaria parasite, he cited this as evidence of irreducible complexity and design. I know little of malarial parasites, but a good synopsis of what Behe claims in The Edge of Evolution and why he is so far off the mark is given here

http://www.sunclipse.org/?p=133

Basically he caims that because two different changes are required for chloroquine resistance, this is evidence for intelligent design. He ignores completely the fact that each change on it's own increases the parasites resistance a little, thus conferring a survival advantage. He also ignores the evidence that chloroquine resistance has arisen independently in Asia and Africa. It seems that he's suggesting that God is an absent-minded dabbler, who, once he had overcome the problem in one location, forgot how he had done it and had to "reinvent his wheel" in another location.


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Trixie
Member (Idle past 2945 days)
Posts: 1011
From: Edinburgh
Joined: 01-03-2004


Message 71 of 102 (652792)
02-16-2012 6:04 AM
Reply to: Message 67 by Genomicus
02-16-2012 4:50 AM


Eh?
Genomicus writes:

Many ID proponents acknowledge that the parts of an IC system can carry out other functions, which means that IC doesn't automatically mean that a given system could not have plausibly evolved.

So ID proponents believe that "irreducibly complex" systems aren't really irreducibly complex? Now that makes no sense. They're still touting it all over the internet as evidence against evolution and for ID, using the common definition which we all know and love.

If what I quoted above is accurate with regard to Behe's current stance, then he has abandoned his own definition of irreducible complexity and embraced what everyone has been telling him for decades. So where does that leave ID now that it's main supporting assertion is dead in the water?

In EofE Behe claimed that the "edge" of evolution was two non-selective mutations in the malarial parasite, conferring chloroquine resistance and calculated erroneous probailites. What he failed to take into account was that each individual mutation could confer increased resistance and so could be selected for. Time and again Behe has done calculations based on no selective advantage for a given mutation. What the Lenski paper does and the chloroquine resistance does is show that his basic assumption on which rests his statistics is wrong so his statistiocs are wrong. Thus his conclusions based on his statistics are wrong.


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Trixie
Member (Idle past 2945 days)
Posts: 1011
From: Edinburgh
Joined: 01-03-2004


Message 74 of 102 (652795)
02-16-2012 6:39 AM
Reply to: Message 70 by Wounded King
02-16-2012 5:49 AM


Re: Deja Vu
Near the bottom of page 429 the authors state

We performed two additional assays to confirm that only phage with all four mutations can infect lamB mutants. The assays were performed using isolates EvoA, F2 and H4 that each had three of the four canonical mutations and D7 that had all four and no others. Only D7 exhibited a measurable adsorption rate on lamB mutants in the medium used in the evolution experiments. These findings indicate an "all or none" form of epistasis among the four mutations responsible for the novel receptor phenotype

From that I take that F2 and H4 did not have the mutation enabling them to use OmpF, but did have the other three. You seem to be suggesting that F2 and H4 had the mutation necessary for OmpF utilisation and no others. I think it means the opposite, but I could be wrong.

Or are we just talking past each other here?


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Trixie
Member (Idle past 2945 days)
Posts: 1011
From: Edinburgh
Joined: 01-03-2004


Message 77 of 102 (652888)
02-16-2012 5:04 PM
Reply to: Message 75 by Wounded King
02-16-2012 8:03 AM


Re: Deja Vu
I think I see the problem. I've expressed myself very badly and given the impression that the mutations have to occur in a specific order. This wasn't my intention, but re-reading my posts I think you're entirely justified in taking that from them. I'll try to be clearer in future.

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Trixie
Member (Idle past 2945 days)
Posts: 1011
From: Edinburgh
Joined: 01-03-2004


(1)
Message 84 of 102 (652978)
02-17-2012 5:02 AM
Reply to: Message 67 by Genomicus
02-16-2012 4:50 AM


Genomicus writes:

Many ID proponents acknowledge that the parts of an IC system can carry out other functions, which means that IC doesn't automatically mean that a given system could not have plausibly evolved.

And yet that's exactly what was proposed in "Of Pandas and People", the book that Dover school board wanted to use in schools. That's what they wanted taught in science class. You're now saying that that was just so much marsh gas. Other "cdesignproponentsists" disagree with you and assert that irreducibly complex systems, by definition, couldn't have evolved. If ID can't even get it's own story straight, why should it be imposed on children who don't yet have enough knowledge to critically examine it's claims? Heck, ID supporters can't even do that!

You are suggesting that Behe's ideas have transmogrifed so much since Dover that we don't recognise them. So does that mean that the "scientific evidence" that he said supported ID and nothing else, no longer exists? If the field is so fluid that it can contradict itself in 7 years, it has no place in a school science class.

On top of that, what caused Behe to change his stance? Is it evidence? Scientific evidence? Is it from his own experimental work or is it from work that was done by others and that was freely available at the time that Behe was busily denying it's existence? In science class we want to give kids scientific information, it's not the place to teach kids the "learning pathway of Behe." Who the hell does he think he is that his painfully slow learning experience should be taught? I'd be rolling around laughing if this wasn't such a serious issue.


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