dishonestly? so you honestly believe that I found this forum and started spewing lies even though I had absolutely nothing to gain by deceiving the people on this forum? Why would I do that? Anything I said on any of my posts, whether I was right or wrong, I at the very least BELIEVED what I was saying.
I think this comes to the heart of the matter. You have answered your own question, why did you come to this site and start relating dishonest lies about what we should expect were evolutionary theory correct? Because you believed what you were saying to be true.
The real question perhaps is why you have a belief in such a warped and twisted version of evolutionary theory? What has led you to think, for example, that evolution considers speciation to be a fish changing into a bird? Did you come by these ideas through being taught evolution in high school or at college? Are you self taught by reading material online, by reading textbooks or journals on evolution?
As you can see, the convergent phylogenies of Geomyidae and Geomydoecus prove that molecular phylogeny is a reliable technique for discerning evolutionary relationships, including the entire history of the evolution of life on Earth as discerned via 16S ribosomal subunit (and other reconstructions.)
Your response? (Please add it to that thread, not this one.)
Why would I do that? Anything I said on any of my posts, whether I was right or wrong, I at the very least BELIEVED what I was saying.
I doubt it. For instance - what are your primary sources for information about the theory of evolution?
If your answer is "creationists have told me what evolution says", then yes, you're being dishonest because you already know that the only honest way to learn about someone's position is from them.
Why give people an excuse by behaving like a child?
At some point, debating with a creationist becomes so pointless that we just try to entertain ourselves. You'll see. (It'll start when you're unable to muster any meaningful response to the convergent phylogenies of Geomyidae and Geomydoecus.)
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.
IMHO, this really isn't in any way the "death knell" for ID in any way whatsoever. ID proponents don't claim that the occurrence of 4 mutations is extremely improbable. The real issue here is whether all four mutations only offered a selective advantage once all four mutations had occurred. If this was the case, then this would be quite a difficulty for the ID folks. But sequence analysis doesn't show in any way that each mutation was in itself non-adaptive. Which means it's not a problem at all for ID. If each mutation conferred some selective advantage to the viruses, then the evolution of OmpF wouldn't be implausible at all, and wouldn't offer a difficulty to ID.
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.
When Behe witters on about irreducible complexity he specifically states that he rejects the idea of incremental improvements finally resulting in a complex change.
Not to my knowledge. For example, in The Edge of Evolution, he discusses the evolution of chloroquine resistance in Plasmodium. He stated that two specific mutations are required to result in chloroquine resistance (whether or not this is indeed the case is, of course, a different matter - I'm just stating my understanding of Behe's position) - yet he accepts that chloroquine resistance evolved without teleology. It seems to me, then, that he accepts the thesis that incremental improvements can result 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.
That is not my understanding of Behe's position. IMO, Behe suggests that it is implausible for an IC system to evolve because it would have to involve a circuitous, indirect Darwinian pathway which is much more improbable than a "direct" Darwinian pathway consisting of gradual improvements on a basic function.
In short, the evolution of this function in these viruses doesn't seem, to me at least, very impressive. It's really not any different than the evolution of chloroquine resistance or the evolution of nylonase.
I guess what it boils down to is that we don't quite agree on what Behe's position is.
I'll respond in more detail if required tomorrow, I'm just in from the movies and very tired.
Take your time - I myself am quite busy so please don't feel rushed.
quote: That is not my understanding of Behe's position. IMO, Behe suggests that it is implausible for an IC system to evolve because it would have to involve a circuitous, indirect Darwinian pathway which is much more improbable than a "direct" Darwinian pathway consisting of gradual improvements on a basic function.
That was his argument, in the days of Darwin's Black Box but I don't think it's his argument now. I think his argument now is that some evolutionary changes require simultaneous mutations (at least two specific mutations) and are too improbable to occur without assistance. The problem with this is showing that the mutations must be simultaneous and I don't think that there are any proven examples yet.
The argument you give above has some serious problems. While the direct pathway might be the simplest means of obtaining a specific result that's really thinking of evolution as working like an intelligent designer - seeking the best way to get to a pre-specified goal. It seems to me more likely that evolution will often follow "indirect" routes because it is NOT goal directed. Looking with hindsight on the probability of the path actually followed is likely no more useful than looking with hindsight on the result of the lottery. And if evolution follows indirect paths we should expect it to reach solutions which can only be found by following indirect paths.
That was his argument, in the days of Darwin's Black Box but I don't think it's his argument now. I think his argument now is that some evolutionary changes require simultaneous mutations (at least two specific mutations)...
Behe acknowledges that if a function requires two specific mutations - each of which are, in themselves, non-adaptive - such a function can evolve. Chloroquine resistance is an example of this, according to him.
The argument you give above has some serious problems...
Umm, I'm not making any argument regarding irreducible complexity. I was merely stating what Behe's position on irreducible complexity is. I wasn't saying that I agree with him.
I actually love a good challenging debate, that is why I come to this site. I can not stand childishness though.
Good, then you will stick around and debate the issues with evidence to substantiate positions.
... so you honestly believe that I found this forum and started spewing lies even though I had absolutely nothing to gain by deceiving the people on this forum? Why would I do that? Anything I said on any of my posts, whether I was right or wrong, I at the very least BELIEVED what I was saying.
So now you know that opinion is often not necessarily related to reality nor able to modify reality in any significant way.
Now you know that some of what you have been taught is incorrect and full of falsehoods, that you have been deluded by false teaching.
Now you have the opportunity to learn what the evidence of reality shows.
Will you take this opportunity? Or will you decide that your personal opinion is more important to you than reality?
This study shows how that is false. Once the final mutation is in place, the others can be lost and the phage will survive.
I get what you say about being tired. Could you please explain what you mean by these two sentences in more detail? As I read them they don't really relate to the results in the paper at all.
As we discussed already in this thread there is no specific final mutation, the order in which the mutations can be acquired varies. The paper certainly doesn't suggest that once the Ompf utilisation trait arises that any of the sites then become unnecessary, and indeed the results would contradict this in many case since they had strains with a heterogenous mix of the 4 different mutation classes including several different forms with 3 mutations none of which showed the ability to utilise Ompf.
You and Genomicus seem to be having essentially the same discussion you and I had starting from Message 13.
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
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.