If you’re going to be a hypocrite, you’re not worth dealing with.

By the way, I “introduced” cooption because cooption is tha basisi of the whole argument of the change from T3SS to flagellum. I have to remind you that the function of T3SS is definitely not the same as the function of the flagellum, so you can in no way have a direct path which simply increases the first function magically arriving at the second.
Anyway, even if I suggested the possibility of intermediate cooptions, just to “increase the credibility of your model, I also took into consideration the simple split between the two existing functions, as you should know if you had read my posts, or if there were no hypocrisy in the world. Here, again, is the relevant part:

“At this point, probably not knowing what else to say, you go back to the concept of gradual fixation. But what are you speaking of? Please explain how you pass from a function (T3SS) to another one (the flagellum) through 490 or so single aminoacid mutations, each one fixed in name of I don’t know what function increase. Are you thinking of, say, 245 gradual mutations improving at single steps the function of the T3SS, and then 245 more single mutations, building gradually the function of the flagellum? What a pity that, of those 490 or so internediaries, there is not a trace, either in existing bacteria, or in fossils, or in general models of protein functions.

Or, if we want to exercise our fantasy (why not? in time I could become a good darwinist) we could split the cake in three: 150 mutations improving T3SS, 150 more to build some new, and then lost, intermediary function (double cooption!), and then 190 to build up the flagellum.”

It’s a good thing that posts are saved in a blog, and we can always look again at what has been said. In spoken language, I have found often people who simply deny what has just happened in the discussion. It’s interesting to find them even in written discussion, but at least here the evidence is under the eyes of all.

Well, I hope this is it at last. Good by, and I really wish you the best.

I am afraid there is no purpose in going on with this discussion with Bob. He goes on changing arguments.

And then how, in your very next post, did you respond to my repeating that you’re assuming no fitness gain for intermediates? You discussed co-option, something which is not part of the argument I was making, and which I wasn’t assuming (I had mentioned gene duplication earlier, but had dropped that line of inquiry because there were more urgent things). It is more than possible for intermediates to have a higher fitness and be carrying out the same function, i.e. for co-option not to be involved.

Yep, thank you for, um, changing the argument.

If you’re going to be a hypocrite, you’re not worth dealing with.

I’d still be interested in seeing how F2XL responds to my criticisms of his maths, but I think he has disappeared.

By the way, while I happily admit that I don’t know the statistical applications you mention (I will try to study something about them, just to know), I still don’t think there is any doubt that statistics is the science which studies random events. Obviously, it is perfectly possible to apply the study of random events to models which make causal assumptions. The fisherian model of hypothesis testing is a good example. There is no doubt that a caual assumtpion is made about the test hypothesis, and that it is evaluated by the statistical anlysis, but that is done indirectly, testing the probability of the nul hypothesis, that is of a randomness hypothesis.

Whatever the sophisticated applications of statistics, there is no doubt that statistics works with statistical distributions, and that statistical distributions are distributions of random events.

Anyway, all my calculations are merely of random probabilities. There is no causal assumption there. I have easily admitted (see my post #192) that if anybody can give a reasonable scenario where all the steps are no more than 2-3 nucleotides far away, and each step can be fixed by NS, then the probability calculations do not apply. I paste here again the relevant part:

“I think that you obviously understand that there is no hope of splitting the transition into 245 or 163 functional intermediates (2-3 mutations steps).

In that case, if you imagine that you can split the transition in such a way, and that each mutation can be fixed quickly, we would be in a scenario similar to the “Methinks it’s like a weasel” example. Indeed, a 2-3 aminoacids coordinated mutation is perfectly accessible to very rapidly dividing beings, like bacteria or malaria parasite, as Behe has clearly shown in his TEOE. We can accept that with prokatyotes, single mutations can be attained easily enough, double ones with a certain ease, given some time, and triple ones probably imply some difficulty, but can be done (especially if you imagine a whole earth covered with proliferating bacteria).”

So, you see, I am admitting that you can find a pathway from T3SS to the flagellum, provided that you can give a model of that kind, and not just imagine it.

I have already said many times the reasons, both logical and empirical, why such a model, IMO, can never exist.

You have never commented about that.

I have almost renounced discussing with you, but just a last attempt.

Both I and F2XL assume that there is no fitness gain during the passage from the original state (T3SS) and the final state. Indeed, I added my calculations to F2XL’s model, because I thought (and still think) that he made an error in the mathematical development.

I must remind you that the T3SS to flagellum scenario has been invented by darwinists to discredit Behe’s concept of IC. Therefore, the T3SS system shiould be the already selected function which is “coopted” to easily pass to the flagellum. Indeed, Miller and Co. just try to convince everybody that, as the proteins for the T3SS are already there, building up the flagellum must certainly be a joke.

F2XL’s model (and mine) are aimed at proving that that is not true. Even if you start from the T3SS, to get the flagellum you still have to traverse an evolutionary path which is practically infinite, and which is equivalent to building up from scratch a new gene of at least 490 nucleotides. So, your concept of “cooption” is completely flawed.

You insist on function gain as though it were a religious observance. But I must remind you that you have no possible path from T3SS to flagellum, that the argument of the IC of the flagellum stays untouched, and that, if you want to find evidence of hundreds of different coopted intermediate functions which can give a start of a model to traverse that landscape you are free to try. Simply, the “evidence” given by Miller about the T3SS does not solve any problem, because even if we acceppt the T3SS as ancestor of the flagellum (which I am not at all ready to do), there remains a huge information gap (at least 490 nucleotides, but again that’s a very generous underestimate) which requires the demonstration of humdreds of new coopted functions, of which there is obviously no trace.

That said, it is obvious that both F2XL’s calculations and mine had only one purpose: to demonstrate that it is absolutely impossible that such an information gap may be traversed by random means alone. Is that clear? The calculations are calculations of the probability that the result be obtained by random variation, nothing else. F2XL’s calculations are (IMO) wrong, but mine (IMO) are not. So, you have to give an answer: do you think that my calculations are right, in the sense that I have correctly calculate the probability that the “traversing” of the 490 nucleotides difference could happen by mere chance? Please, answer.

If your answer is no, please show where is the mathematical error. Don’t avoid the question citing again the problem of function gain. That will come after.

If your answer is yes, then let us be clear: you are admitting that the passage from T3SS to flagellum could never happen by chance alone, because its probability is vastly below Dembski’s UPB.

That’s the first question.

Once you have admitted that my calculations are right (or, in alternative, shown why they are wrong), then we can speak of the assumptions of function gain or not gain.

Indeed, I have discussed that in detail in the cited posts, and you have never commented. So, for you comfort, I paste here the more relevant parts.

From post 155:

When we ask for a path, we are asking for a path, not a single (or double) jump from here to almost here.

I will be more clear: we need a model for at least two scenarios:

1) A de novo protein gene. See for that my detailed discussion in the relevant thread. De novo protein genes, which bear no recognizable homology to other proteins, are being increasingly recognized. They are an empirical fact, and they must be explained by some model. The length of these genes is conspicous (130 aminoacids in the example discussed on the thread). The search space huge. Where is the traversing apparatus? What form could it take?

2) The transition from a protein with a function to one other with another function, where the functions are distinctly different, and the proteins are too. Let’s say that they present some homology, say 30%, which lets darwinist boast that one is the ancestor of the other. That’s more or less the scenario for some proteins in the flagellum, isn’t it? Well we still have a 70% difference to explain. That’s quite a landscape to traverse, and the same questions as at point 1) apply.

You cannot explain away these problems with examples of one or two muations bearing very similar proteins, indeed a same protein with slightly different recognition code. It is obvious hat even a single aminoacid can deeply affect recognition.

You must explain different protein folding, different function (not just the same function on slightly different ligands), different protein assembly. That’s the kind of problems ID has always pointed out. Behe is not just “shifting the goalposts”. The goalposts have never been there. One or two aminoacid jumps inside the same island of functionality have never been denied by anyone, either logically or empirically. They are exactly the basic steps which you should use to build your model pathway: they are not the pathway itself.

Let’s remember that Behe, in TEOE, places exactly at two coordnated aminoacid mutations the empirical “edge”, according to his reasonings about malaria parasite mutations. You can agree or not, but that is exactly his view. He is not shifting anything.

From post 184:

At this point, probably not knowing what else to say, you go back to the concept of gradual fixation. But what are you speaking of? Please explain how you pass from a function (T3SS) to another one (the flagellum) through 490 or so single aminoacid mutations, each one fixed in name of I don’t know what function increase. Are you thinking of, say, 245 gradual mutations improving at single steps the function of the T3SS, and then 245 more single mutations, building gradually the function of the flagellum? What a pity that, of those 490 or so internediaries, there is not a trace, either in existing bacteria, or in fossils, or in general models of protein functions.

Or, if we want to exercise our fantasy (why not? in time I could become a good darwinist) we could split the cake in three: 150 mutations improving T3SS, 150 more to build some new, and then lost, intermediary function (double cooption!), and then 190 to build up the flagellum.

Obviously, all that would happen in hundreds of special “niches”, each of it with a special fitness landscape, so that we can explain the total diappearance of all those intermediary “functions” form the surface of our planet!

Do you really believe all that?

From post 192:

Patrick:

I think that you obviously understand that there is no hope of splitting the transition into 245 or 163 functional intermediates (2-3 mutations steps).

In that case, if you imagine that you can split the transition in such a way, and that each mutation can be fixed quickly, we would be in a scenario similar to the “Methinks it’s like a weasel” example. Indeed, a 2-3 aminoacids coordinated mutation is perfectly accessible to very rapidly dividing beings, like bacteria or malaria parasite, as Behe has clearly shown in his TEOE. We can accept that with prokatyotes, single mutations can be attained easily enough, double ones with a certain ease, given some time, and triple ones probably imply some difficulty, but can be done (especially if you imagine a whole earth covered with proliferating bacteria). The scenario would change dramatically, in the sense of impossibility, for bigger and slower animals, like mammals.

But let’s stick to bacteria. The fact is, there are only two ways of splitting the path in 2-3 nucleotide changes:

a) You need hundreds of intermediates, all of them with progressively increasing function of some type, all neatly ordered in the pathway which brings to the final flagellum. Each of them must have reproductive advantage enough so that it can be fixed.

b) You know which are the ciorrect nucleotides, and you artificially fix them when they appear. That’s the case of “Methinks it’s like a weasel”. You already have the information, and you just select it.

As the option b) is obviously design, let’s discuss option a). Again, it is not an option, for 3 different reasons:

1) Logical: there is no reason that in a search space functions can be so strictly and magically realated. There is no mathematical model which can anticipate such a structure. Indeed, if it existed, that would be heavy evidence for tha existence of God. Moreover, protein functions derive from totally empirical phenomena, like protein folding in a number of very different domains, and there is really no logical reasons that a ladder of intermidiate functions can “lead” from one function to a different one, and not only in a single lucky case, but practically in all cases.

2) Empirical: That process, or model, has never been onserved. The examples cited by Bob are definitely not examples of the splitting of a function in intermediate steps, but rather of single steps leading from one function to a slight variation of the same function.

3) Empirical (again): if the final function is reached through hundreds of intermediate functions, all of them selected and fixed, where are all those intermediates now? Why do we observe only the starting function (bacteria with T3SS) and the final function (bacteria with flagella)? Where are the intermediates? If graduality and fixation are what happens, why can’t we observe any evidence of that? In other words, we nedd literally billions of billions of molecular intermediates, which do not exist. Remember that the premise is that each successive step has greater fitness than the previous. Where are those steps? Where are those successful intermediates? were they erased by the final winner, the bacterium with flagellum? But then, why can we still easily observe the ancestor without flagella (and , obviously, without any of the amazing intermediate and never observed functions)?

So, where are your detailed answers and comments to all that? If you don’t want to discuss, just say that. If you have your model of function gain in this specific scenarion, please describe it. Do whatever you please. I have said all that I could reasonably say.

The fitness gain assumption is important, because otherwise you’re just calculating the proportion of the parameter space that could be explored. But, if there is a fitness gain of intermediates, this is an irrelevant calculation, because it will say little to nothing about the probability of the target being reached. It is, I believe, because of this that Dr. Dembski has been working so much on evolutionary informatics.

…statistics is the science of random events, not of causal assumptions.

Sorry, this is just wrong. A lot of modern-day statistics is about causal models. Look up topics like structural equation modelling, path analysis, graphical models etc.

I am afraid there is no purpose in going on with this discussion with Bob. He goes on changing arguments. F2XL’s calculations are wrong because they are statistically not correct. My calculations are wrong because I assume no fitness gain. I really think he is not fair at all.

He has never, never said if he thinks that my calculations are right or wrong from a statistical point of view: that has obviously nothing to do with the fitness gain assumption, because, as I have tried to explain to him (although he probably already knows), statistics is the science of random events, not of causal assumptions. But everything is useless.

Instead, I would really appreciate F2XL’s feedback on the problem of the calculations, because I feel that it is not right to leave it open.

So, I will stay tuned on this old thread, in case someone has to say something pertinent.

you assume with absolutely no evidence whatsoever that intermediates have no fitness gain.

Name the functional intermediates in the indirect pathway.

Also, since when did “intermediates” and “fitness gain” have anything to do with calculating informational bits? You seem to have your own definition of CSI. Or you seem to be asserting that the casual history must be known. F2XL and gpuccio are calculating the probability of an indirect pathway…NOT the informational bits of the flagellum! Bob, that is one giant basic misunderstanding.

I cover calculating CSI over at Overwhelming Evidence. But I’ll make it short here. In order to calculate the informational bits used to represent my name “Patrick” you consider that each letter has an information capacity of 8 bits. So the calculation is simple: 8 bits X 7 letters = 56 informational bits.

In the same way, each “letter” of the DNA has an information capacity of 2 bits. The DNA sequence in the genome encodes to 42 proteins in the flagellum. So in order to calculate the informational bits for the flagellum: 2 bits X xxx letters = xxx informational bits. I did not look up the number of letters in the sequence, but that gives the basic idea.

I should state the caveat that no one currently knows the exact information content and that this is the MINIMUM information since my estimate would only include genes. We’re still attempting to comprehend the language conventions of the biological code. MicroRNA, etc. would certainly add to the information content for all biological systems. An analogy to computers is how XML, meta tags, and Dynamic Linking Libraries add to the core code (and thus informational content) of a program. I would also refer people back to comment #70 that covers other issues. This is perhaps why ID proponents are shy to provide this calculation since it’s not final and since a lower estimate “might” be less than 500 (Dembski’s UPB). But as I noted I did not look up the sequence although I remember there being at least 50 genes involved.

Your own calculation are also wrong for the obvious reason that you assume with absolutely no evidence whatsoever that intermediates have no fitness gain.

“If I’m wrong, you would do better to work through my argument and show where and why it’s wrong. At the moment you’re reduced to repeating yourself because you’re not applying yourself to my arguments.”

Excuse me, but I am repeating myself because, in the last few days, you gave me not only no argument, but indeed no answer.

In the old post #183 you just cite again the possibility of fixation. I have answered in detail to that (see for instance my post #155, 184 and 192), giving very detailed arguments, about which you have never commented.

Your only two more recent posts (#193 and 194) were answers to F2XL, and did not address in any way my calculations. Your strange behaviour seems to be: post to F2XL to say: “Hey, your calculations are wrong!” (true, but you have not understood why); and then post to me and say nothing of ny calculations (should I believe you suspect they are right?), and generically citing again the problem of gradual selection, without supporting it in any way, and without addressing the specific objections I have given at least three times in the recent history of this thread, in posts specifically addressed to you (once to Patrick, to be precise).

To be clear, the two problems are completely separate: the possibility of selection has nothing to do with the calculation of a probability. Although many forget that, statistics can be applied only to random phenomena, to analyze them or, sometimes, to exclude them. If there is a non random cause, probabilities don’t apply.

So, the possibility of gradual selection has to be ruled out or affirmed on a different level (logical and empirical), but not by probabilistic calculations. I have tried to discuss that, and you have not answered.

Instead, the possibility of random causes in each specific context or model have to be evaluated by a correct calculation of probabilities. I have tried to do that for our specific model, and you have never been kind enough to say if you believe I am right or wrong, or at least if you can’t make up your mind.

So, let’s comment your last (and only) “argument”, which I could not comment before because it’s in your last post. I suppose it should be contained in the following phrase:

“That would be true if it were the probability that there was at least one mutation at the locus in a given time, and that the final mutation was to the “correct” base. However, what is calculated is clearly not that: it’s lacking some vital constituents (like a mutation rate).”

Would that be an argument? I scarcely can understamd what it means. Bu I will comment it just the same, in case you are expecting to accuse me of not replying…

First of all, my calculations to which you refer are exactly what is needed in the model we were discussing, that is “the probability that there was at least one mutation at the locus in a given time, and that the final mutation was to the “correct” base.”, or, to put it better (your phrase is rather obscure), they calculate the probability that the final mutation, after the minimum number of events (490) which can generate a 490 nucleotide mutation, can give the correct base at each of the 490 sites. That corresponds to p^490.

Then you say:

“However, what is calculated is clearly not that: it’s lacking some vital constituents (like a mutation rate).”

What argument would that be? The calculation of a probability does not need any vital constituents: it just needs qunatitative data and context (model). A mutation rate is part of the model, but it must be taken into account after you have calculated the porbability of the events which the mutations should generate. So, if that can be called an argument, it’s just wrong.

Anyway, just to repeat myself for the nth time, in my post #190 I have given a simpler and more correct (IMO) way to calculate the probabilities in our discussed model, and I have also taken into account the probabilistic resources implied in the model (including the mutation rate). The result? No comment from you…

The probability p has to be multiplied if we want to have the probability of more combined mutations.

That would be true if it were the probability that there was at least one mutation at the locus in a given time, and that the final mutation was to the “correct” base. However, what is calculated is clearly not that: it’s lacking some vital constituents (like a mutation rate).

If I’m wrong, you would do better to work through my argument and show where and why it’s wrong. At the moment you’re reduced to repeating yourself because you’re not applying yourself to my arguments.