Do we know if the 3 intermediate mutations before the fourth really 'useful' one added any benefits of their own to the organism?
The original paper does touch on this, although it doesn't provide a definitive answer. They say ...
Meyer et al., 2012 writes:
However, the all-or-none epistasis among the mutations means that selection for that new capacity per se was not responsible for the rise of the three prior mutations. Nonetheless, there are several lines of evidence that selection drove their rise.
They go on to describe evidence such as the ratio of synonymous to non-synonymous mutations, the distribution of those mutations in the protein principally being concentrated around the region which interacts with the LamB receptor and the fact that there is a much higher level of parallel evolution amongst the strains that evolved to utilise OmpF (61% in these as opposed to 17% in those that only utilised LamB).
It worth noting that while all of their evolved strains that could utilise OmpF did have 4 mutations they weren't all the same 4 mutations. In fact only 2 mutations were shared by all of the OmpF capable strains. The other 2 were slightly broader classes of mutations in one case all affecting the same amino and in the other being restricted between amino acids 990-1000 of the J protein. These distinctions would certainly heavily affect your probability calculations and it is highly likely that this is not a comprehensive catalogue of all the variations that give rise to the OmpF infection trait.
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.
I don't think the sort of strict sequentiality you seem to be describing here really exists.
What the author's conclude is that all 4 mutations are required, the order in which they arise seems irrelevant. In their replicate experiments all of the mutation types arose in the non OmpF infecting strains and at least 2 distinct combinations of 3 mutations arose, in EvoA lacking the A3034G mutation and in F2 and H4 lacking the G3319A mutation. Both of these were just one mutation away from an OmpF infective strain through slightly different evolutionary trajectories.
No doubt it is significant that in both cases it is one of the highly specific mutations that is missing but there is no reason to assume that with a broader sampling strains might not have been found with both the highly specific mutations but lacking one of the broader mutations, such strains are just more unlikely.
Your final point comes back to the lamentable lability of the term 'Irreducible Complexity' which seems to be one of those terms that means whatever a person wants it to mean. Behe himself has given more than 1 distinctly different definition and the main point of difference is precisely whether systems which have prior functional intermediates with a distinct function, as in this case, are IC.
It would certainly be very informative to have some proper analysis of the extent and nature of the fitness benefits of each mutation in isolation. Perhaps all any of the mutations do is increase affinity for LamB up until such a point with all 4 mutations that it can now bind to OmpF which is apparently the most structurally similar E. coli protein to LamB (at least going by crystal structure).
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?
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.
If you mean that the A3034G mutations never arose without the 3 other mutation classes having already occurred then this is incorrect as can be seen from strains F2 and H4 in fig 3. You seem to be basing your whole analysis on fig 2 covering the initial experiment and ignoring fig 3 which shows the wider range of mutations in both the 'ancestral range' and OmpF utilising strains from their larger scale replay experiments.
Looking back at the paper I wonder if their claim ...
Meyer et al., 2012 writes:
In the λ population that evolved to use OmpF in the initial experiment, the A3034G mutation was the fourth and final step
... is really substantiated by the results. After all, these strains were all evolving in parallel and the data don't provide any sort of time course, beyond the initial ancestral strain as a t0, the evolved strains assayed were collected on the same day. So what they are really saying is that for the EvoA strain to become OmpF competent A3034G would be the last required mutation. There isn't actually any evidence presented as to the order the mutations actually occurred in the EvoC strain or in any of the replay strains. This is a shame since from the way they describe their protocol this is data they could have collected.
This study does not report that all four mutations must arise simultaneously in order to confer a selective advantage. Indeed, it could be that each mutation conferred some selective advantage.
This is in fact what the paper suggests, they note several features of the 'prior' mutations in the strains that cannot use OmpF that would indicate that they are subject to positive selection.
Possibly, we're not communicating very well, though.
This seems to be the case, and it is certainly not helped by the fact the Irreducible Complexity has had more than one definition. I think part of the problem is that people are mixing up the figure for the evolution of the Chloroquine complex of mutations, which as you say came from someone else's previous work, with Behe's subsequent use of this as a basis for predicting the likely frequency of more complex compound mutations.
This is why I keep asking you to be more specific. There is no 'the mutation necessary for OmpF utilisation' what is needed is all four mutations.
The way you describe it is that there are three intermediary mutations which then potentiate a final specific fourth mutation which actually confers the ability to utilise OmpF. But the evidence suggests that this is not what happens, there are a spectrum of mutations which occur and all four mutations of particular types are required for OmpF utilisation. But these are arising independently, there is nothing to suggest that they need to occur in any specific order.
What H4 and F2 both have is the A3034G mutation which is what I assumed you meant when you said 'the fourth mutation never occurred without the others', since it is the difference between the EvoA and EvoC strains in fig.2. If you actually told me what mutation you meant it would make things a lot simpler, but as far as I can tell none of the mutations would fit your description of requiring the other three before it could occur.
So what mutation, specifically, were you talking about?