Does gpuccio’s argument that 500 bits of Functional Information implies Design work?

On Uncommon Descent, poster gpuccio has been discussing “functional information”. Most of gpuccio’s argument is a conventional “islands of function” argument. Not being very knowledgeable about biochemistry, I’ll happily leave that argument to others.

But I have been intrigued by gpuccio’s use of Functional Information, in particular gpuccio’s assertion that if we observe 500 bits of it, that this is a reliable indicator of Design, as here, about at the 11th sentence of point (a):

… the idea is that if we observe any object that exhibits complex functional information (for example, more than 500 bits of functional information ) for an explicitly defined function (whatever it is) we can safely infer design.

I wonder how this general method works. As far as I can see, it doesn’t work. There would be seem to be three possible ways of arguing for it, and in the end; two don’t work and one is just plain silly. Which of these is the basis for gpuccio’s statement? Let’s investigate …

A quick summary

Let me list the three ways, briefly.

(1) The first is the argument using William Dembski’s (2002) Law of Conservation of Complex Specified Information. I have argued (2007) that this is formulated in such a way as to compare apples to oranges, and thus is not able to reject normal evolutionary processes as explanations for the “complex” functional information.  In any case, I see little sign that gpuccio is using the LCCSI.

(2) The second is the argument that the functional information indicates that only an extremely small fraction of genotypes have the desired function, and the rest are all alike in totally lacking any of this function.  This would prevent natural selection from following any path of increasing fitness to the function, and the rareness of the genotypes that have nonzero function would prevent mutational processes from finding them. This is, as far as I can tell, gpuccio’s islands-of-function argument. If such cases can be found, then explaining them by natural evolutionary processes would indeed be difficult. That is gpuccio’s main argument, and I leave it to others to argue with its application in the cases where gpuccio uses it. I am concerned here, not with the islands-of-function argument itself, but with whether the design inference from 500 bits of functional information is generally valid.

We are asking here whether, in general, observation of more than 500 bits of functional information is “a reliable indicator of design”. And gpuccio’s definition of functional information is not confined to cases of islands of function, but also includes cases where there would be a path to along which function increases. In such cases, seeing 500 bits of functional information, we cannot conclude from this that it is extremely unlikely to have arisen by normal evolutionary processes. So the general rule that gpuccio gives fails, as it is not reliable.

(3) The third possibility is an additional condition that is added to the design inference. It simply declares that unless the set of genotypes is effectively unreachable by normal evolutionary processes, we don’t call the pattern “complex functional information”. It does not simply define “complex functional information” as a case where we can define a level of function that makes probability of the set less than 2^{-500}.  That additional condition allows us to safely conclude that normal evolutionary forces can be dismissed — by definition. But it leaves the reader to do the heavy lifting, as the reader has to determine that the set of genotypes has an extremely low probability of being reached. And once they have done that, they will find that the additional step of concluding that the genotypes have “complex functional information” adds nothing to our knowledge. CFI becomes a useless add-on that sounds deep and mysterious but actually tells you nothing except what you already know. So CFI becomes useless. And there seems to be some indication that gpuccio does use this additional condition.

Let us go over these three possibilities in some detail. First, what is the connection of gpuccio’s “functional information” to Jack Szostak’s quantity of the same name?

Is gpuccio’s Functional Information the same as Szostak’s Functional Information?

gpuccio acknowledges that gpuccio’s definition of Functional Information is closely connected to Jack Szostak’s definition of it. gpuccio notes here:

Please, not[e] the definition of functional information as:

“the fraction of all possible configurations of the system that possess a degree of function >=
Ex.”

which is identical to my definition, in particular my definition of functional information as the
upper tail of the observed function, that was so much criticized by DNA_Jock.

(I have corrected gpuccio’s typo of “not” to “note”, JF)

We shall see later that there may be some ways in which gpuccio’s definition
is modified from Szostak’s. Jack Szostak and his co-authors never attempted any use of his definition to infer Design. Nor did Leslie Orgel, whose Specified Information (in his 1973 book The Origins of Life) preceded Szostak’s. So the part about design inference must come from somewhere else.

gpuccio seems to be making one of three possible arguments;

Possibility #1 That there is some mathematical theorem that proves that ordinary evolutionary processes cannot result in an adaptation that has 500 bits of Functional Information.

Use of such a theorem was attempted by William Dembski, his Law of Conservation of Complex Specified Information, explained in Dembski’s book No Free Lunch: Why Specified Complexity Cannot Be Purchased without Intelligence (2001). But Dembski’s LCCSI theorem did not do what Dembski needed it to do. I have explained why in my own article on Dembski’s arguments (here). Dembski’s LCCSI changed the specification before and after evolutionary processes, and so he was comparing apples to oranges.

In any case, as far as I can see gpuccio has not attempted to derive gpuccio’s argument from Dembski’s, and gpuccio has not directly invoked the LCCSI, or provided a theorem to replace it.  gpuccio said in a response to a comment of mine at TSZ,

Look, I will not enter the specifics of your criticism to Dembski. I agre with Dembski in most things, but not in all, and my arguments are however more focused on empirical science and in particular biology.

While thus disclaiming that the argument is Dembski’s, on the other hand gpuccio does associate the argument with Dembski here by saying that

Of course, Dembski, Abel, Durston and many others are the absolute references for any discussion about functional information. I think and hope that my ideas are absolutely derived from theirs. My only purpose is to detail some aspects of the problem.

and by saying elsewhere that

No generation of more than 500 bits has ever been observed to arise in a non design system (as you know, this is the fundamental idea in ID).

That figure being Dembski’s, this leaves it unclear whether gpuccio is or is not basing the argument on Dembski’s. But gpuccio does not directly invoke the LCCSI, or try to come up with some mathematical theorem that replaces it.

So possibility #1 can be safely ruled out.

Possibility #2. That the target region in the computation of Functional Information consists of all of the sequences that have nonzero function, while all other sequences have zero function. As there is no function elsewhere, natural selection for this function then cannot favor sequences closer and closer to the target region.

Such cases are possible, and usually gpuccio is talking about cases like this. But gpuccio does not require them in order to have Functional Information. gpuccio does not rule out that the region could be defined by a high level of function, with lower levels of function in sequences outside of the region, so that there could be paths allowing evolution to reach the target region of sequences.

An example in which gpuccio recognizes that lower levels of function can exist outside the target region is found here, where gpuccio is discussing natural and artificial selection:

Then you can ask: why have I spent a lot of time discussing how NS (and AS) can in some cases add some functional information to a sequence (see my posts #284, #285 and #287)

There is a very good reason for that, IMO.

I am arguing that:

1) It is possible for NS to add some functional information to a sequence, in a few very specific cases, but:

2) Those cases are extremely rare exceptions, with very specific features, and:

3) If we understand well what are the feature that allow, in those exceptional cases, those limited “successes” of NS, we can easily demonstrate that:

4) Because of those same features that allow the intervention of NS, those scenarios can never, never be steps to complex functional information.

Jack Szostak defined functional information by having us define a cutoff level of function to define a set of sequences that had function greater than that, without any condition that the other sequences had zero function. Neither did Durston. And as we’ve seen gpuccio associates his argument with theirs.

So this second possibility could not be the source of gpuccio’s general assertion about 500 bits of functional information being a reliable indicator of design, however much gpuccio concentrates on such cases.

Possibility #3. That there is an additional condition in gpuccio’s Functional Information, one that does not allow us to declare it to be present if there is a way for evolutionary processes to achieve that high a level of function. In short, if we see 500 bits of Szostak’s functional information, and if it can be put into the genome by natural evolutionary processes such as natural selection then for that reason we declare that it is not really Functional Information. If gpuccio is doing this, then gpuccio’s Functional Information is really a very different animal than Szostak’s functional information.

Is gpuccio doing that? gpuccio does associate his argument with William Dembski’s, at least in some of his statements.  And William Dembski has defined his Complex Specified Information in this way, adding the condition that it is not really CSI unless it is sufficiently improbable that it be achieved by natural evolutionary forces (see my discussion of this here in the section on “Dembski’s revised CSI argument” that refer to Dembski’s statements here). And Dembski’s added condition renders use of his CSI a useless afterthought to the design inference.

gpuccio does seem to be making a similar condition. Dembski’s added condition comes in via the calculation of the “probability” of each genotype. In Szostak’s definition, the probabilities of sequences are simply their frequencies among all possible sequences, with each being counted equally. In Dembski’s CSI calculation, we are instead supposed to compute the probability of the sequence given all evolutionary processes, including natural selection.

gpuccio has a similar condition in the requirements for concluding that complex
functional information is present:  We can see it at step (6) here:

If our conclusion is yes, we must still do one thing. We observe carefully the object and what we know of the system, and we ask if there is any known and credible algorithmic explanation of the sequence in that system. Usually, that is easily done by excluding regularity, which is easily done for functional specification. However, as in the particular case of functional proteins a special algorithm has been proposed, neo darwininism, which is intended to explain non regular functional sequences by a mix of chance and regularity, for this special case we must show that such an explanation is not credible, and that it is not supported by facts. That is a part which I have not yet discussed in detail here. The necessity part of the algorithm (NS) is not analyzed by dFSCI alone, but by other approaches and considerations. dFSCI is essential to evaluate the random part of the algorithm (RV). However, the short conclusion is that neo darwinism is not a known and credible algorithm which can explain the origin of even one protein superfamily. It is neither known nor credible. And I am not aware of any other algorithm ever proposed to explain (without design) the origin of functional, non regular sequences.

In other words, you, the user of the concept, are on your own. You have to rule out that natural selection (and other evolutionary processes) could reach the target sequences. And once you have ruled it out, you have no real need for the declaration that complex functional information is present.

I have gone on long enough. I conclude that the rule that observation of 500 bits of functional information is present allows us to conclude in favor of Design (or at any rate, to rule out normal evolutionary processes as the source of the adaptation) is simply nonexistent. Or if it does exist, it is as a useless add-on to an argument that draws that conclusion for some other reason, leaving the really hard work to the user.

Let’s end by asking gpuccio some questions:
1. Is your “functional information” the same as Szostak’s?
2. Or does it add the requirement that there be no function in sequences that
are outside of the target set?
3. Does it also require us to compute the probability that the sequence arises as a result of normal evolutionary processes?

907 thoughts on “Does gpuccio’s argument that 500 bits of Functional Information implies Design work?

  1. DNA_Jock,

    He (gpuccio) can’t calculate the FI for an optimized protein (since other peaks exist), but no matter, as that FI value is irrelevant. You guys need to calculate the proportion of sequences that carry a minimally selectable function (and not necessarily the function you are measuring, just one that can lead to the function of interest).

    What the Hayashi paper is telling us is that the minimum selectable function is on a different island then the wild type. What we are observing is the wild type.

    What gpuccio is observing are proteins that are mutationally resistant and again far away from a random sequence. The measure he is making is solid as it is consistently showing proteins in islands far away from random sequences as they have achieved a mutationally sensitive state.

    You guys need to calculate the proportion of sequences that carry a minimally selectable function (and not necessarily the function you are measuring, just one that can lead to the function of interest)

    Not unless minimal detectable function has a realistic mutational path to the observed wild type or mutationally sensitive protein.

    Gpuccio has no idea whatsoever about how to do that, so he has decided to not even try. He would rather simply declare victory.

    It’s the best current method that I have seen.

    Humm. How reliably, and why?

    So you have evidence that life can be sustained without reliable cell division?

    A coupla different prokaryotes, perhaps? Applying your tornado-in-a-junkyard math to endosymbiosis seems like a poor tactical choice, mate.

    A 747 has a much better chance then a couple of prokaryotes that are missing a spliceosome, a nuclear pore complex, a golgi apparatus, chromosome structure, a ubiquitin system and then have the ability to reproduce all these structures reliably.

    How about a tornado in a junkyard producing a 747 that can self replicate:-)

  2. Rumraket,

    The archaeal and bacterial ancestors of eukaryotes were capable of cell division. What’s the problem?

    The first problem is you are begging the question.

    There is almost no evidence that this transition is possible from cell division alone and no preexisting spliceosome, nuclear pore complex, ubiquitin system etc for endosymbiosis .

  3. colewd: The first problem is you are begging the question.

    No it’s not begging the question, prokaryotes ARE capable of cell division.

    There is almost no evidence that this transition is possible from cell division alone and no preexisting spliceosome, nuclear pore complex, ubiquitin system etc for endosymbiosis.

    There is not only evidence it is possible, the evidence that exists is evidence that it actually happened.

    And Bill these systems aren’t “replicated” at cell division, it’s not like something copies every single ribosome and then the cell divides. The organelles and molecules in the cell are simply dividided amongst the daughter cells. Once cell division has happened, the two resulting cells are smaller, but grow again as more molecules and organelles are synthesized by the inherited ribosomes.

  4. Rumraket,

    No it’s not begging the question, prokaryotes ARE capable of cell division.

    Yes, your right they can perform cell division but this is not why you are begging the question.

    You are assuming that they are ancestors of eukaryotic cells when you have no realistic transitional path to support this assumption.

  5. Rumraket,

    There is not only evidence it is possible, the evidence that exists is evidence that it actually happened.

    What evidence? You need millions of bits of functional information. How was it generated?

  6. colewd: You are assuming that they are ancestors of eukaryotic cells when you have no realistic transitional path to support this assumption.

    What’s unrealistic about symbiosis? Gene duplications and point mutations? I don’t see what the problem is at all.

  7. colewd: What evidence?

    That simpler versions of these things exist in prokaryotes. The fact that many of them seem to have become larger and more complex (like the spliceosome and ubiquitylation systems) in large part by multiple duplications over time.

    You need millions of bits of functional information. How was it generated?

    Millions of bits for what? Please do that calculation for me. What are these entities that add up to millions of bits of FI?

    Regardless, are you saying that in so far as we don’t know what the ancestral state was, it was designed?

  8. Mung: I don’t think anyone can be faulted for thinking that FI is a measure of information.

    I saw a remark on references to -\!\log_2 p as information, perhaps from Marks at ENV, perhaps from Marks, Dembski, and Ewert in their book — I’m not going to run it down now — that ran to the effect of “everybody does it.” That may be the case. But I don’t think it’s an acceptable excuse.

    In a quick reading of Hazen (2009), I found some of the “right words” about information, sprinkled here and there, but failed to get from them an understanding of how “functional information” plays the role of information in physical systems.

    Szostak (2003) started out considering “informational molecules,” and thus easily associated a measure of “information” with them at the verbal level. But I don’t see what the “information” that we measure on a specified ensemble of molecules has to do with the informational role that the molecules themselves play in certain physical contexts. I’m thinking now that Hazen et al. (2007) were able to generalize as they did precisely because there was no connection.

    I’m thinking also that the only way to make sense of “functional information” as information is in terms of a process sampling the space of configurations of a physical system. Then gain of information is clearly associated with the sampling process, not with the configurations in the sample space. (If Szostak were to say, “That’s what I had in mind,” then my response would be, “You need to make the process explicit in the formalism.”) From an ID perspective, this would be a huge change, because it would be clear that the process gains information by sampling configurations, and does not create information in the configurations.

  9. colewd,
    I wrote

    He (gpuccio) can’t calculate the FI for an optimized protein (since other peaks exist), but no matter, as that FI value is irrelevant. You guys need to calculate the proportion of sequences that carry a minimally selectable function (and not necessarily the function you are measuring, just one that can lead to the function of interest).

    To which you responded

    What the Hayashi paper is telling us is that the minimum selectable function is on a different island then the wild type. What we are observing is the wild type.

    Your bit about the wild type there is Texas Sharp Shooter. Please, get a grip.
    But let’s explore what the Hayashi paper is telling us, especially with regard to the “minimum selectable function ” :-

    First, the smooth surface of the mountainous structure from the foot to at least a relative fitness of 0.4 means that it is possible for most random or primordial sequences to evolve with relative ease up to the middle region of the fitness landscape by adaptive walking with only single substitutions.

    Personally, I think they are over-concluding here. I would be happy with the conclusion that 1 – 10% of random sequences can do this, rather than “most”. Hayashi actually reckons that there is more land than sea in the ‘isolated islands’ metaphor. I disagree.
    Anyhoo, Hayashi is telling us that minimally selectable function is easily accessible to random walks. This is, in fact, the total death knell for gpuccio’s argument.
    Moving on.
    If you actually look at a Hayashi landscape, you’ll also realize that the failure to find the wild type is expected, and unimportant. The “minimal selectable function” is on ALL islands. It’s the definition of “above sea level”, FFS. They did not sample anything like enough sequences to determine whether any of the islands they did find were the same as the island that harbors the wild-type. There are thousands and thousands of craggy peaks, and no reason to think that the observed wild type is particularly easily accessible. They had no trouble AT ALL finding sequences that were good enough.
    You wrote

    What gpuccio is observing are proteins that are mutationally resistant and again far away from a random sequence. The measure he is making is solid as it is consistently showing proteins in islands far away from random sequences as they have achieved a mutationally sensitive state.

    Gpuccio is studying exclusively ‘proteins that are mutationally resistant’. They are highly optimized; they have co-evolved over millenia with other proteins. Their mutational sensitivity is entirely unrelated to the mutational sensitivity of the proteins whence they came.
    The phrase “far away from a random sequence” is incoherent. Perhaps you meant “far away from the average level of function of random sequences”. I could go along with that.

    Not unless minimal detectable function has a realistic mutational path to the observed wild type or mutationally sensitive protein.

    It does.
    Cuz I say so.
    See, I can confidently assert things too. But if you want anyone to pay attention to your ID-math, the burden is on you to support your claim that these paths do not exist. Good luck.
    (BTW, what evidence we have is on my side here. See Keefe & Szostak, 2001; McLaughlin et al, 2012, etc., etc.)

    So you have evidence that life can be sustained without reliable cell division?

    ROFL. You were claiming that eukaryotic cell division requires that the cell be able to reliably make PRP8 spliceosome protein, and always has. I repeat my question: How reliably, and why?

    A 747 has a much better chance then a couple of prokaryotes that are missing a spliceosome, a nuclear pore complex, a golgi apparatus, chromosome structure, a ubiquitin system and then have the ability to reproduce all these structures reliably.

    Please show your working.
    You’ll need to take into account the prokaryotes ability to replicate with variation.
    Again, good luck with that.

  10. Rumraket,

    That simpler versions of these things exist in prokaryotes. The fact that many of them seem to have become larger and more complex (like the spliceosome and ubiquitylation systems) in large part by multiple duplications over time.

    There are 200 unique proteins in the spliceosome. How would gene duplication account for these. Gene duplication followed by mutation would generally break down a sequence.

    Millions of bits for what? Please do that calculation for me. What are these entities that add up to millions of bits of FI?

    Regardless, are you saying that in so far as we don’t know what the ancestral state was, it was designed?

    All the systems I mentioned have more then 500k AA’s. We can quibble over how much FI that is but I think we can agree that it is more then 500 bits.

    The design inference is based on the observation of FI in biology. There is no real reason to believe that the ancestral state is different then it is today other then trying to make the simple to complex model work.

    If we look at the minimum requirement for life it includes cell division. This is a very precise and complex process which excludes the idea of a simple beginning.

  11. DNA_Jock,

    Your bit about the wild type there is Texas Sharp Shooter. Please, get a grip.

    The wild type is what we are observing. Hayashi estimated a library of 10^70 sequences to get there. There are less then 10^50 trials in all of life’s history.

    We are observing preserved sequences from species that split billions of years ago.

    There is no fallacy here it is simply an observation that is confirming the design inference.

    It does.
    Cuz I say so.
    See, I can confidently assert things too. But if you want anyone to pay attention to your ID-math, the burden is on you to support your claim that these paths do not exist. Good luck.

    The existence of these paths is an evolutionist claim. There is no reason for them to exist and no experimental data showing they exist. Your attempt at a burden shift is duly noted.

    ROFL. You were claiming that eukaryotic cell division requires that the cell be able to reliably make PRP8 spliceosome protein, and always has. I repeat my question: How reliably, and why?

    Do you have evidence of a eukaryotic cell operating without a PRP 8 protein? The accuracy observed is less then 1 in 10^10 errors per cell division.

    Please show your working.
    You’ll need to take into account the prokaryotes ability to replicate with variation.

    I think you need to show that replication and variation can generate FI. So far the evidence does not favor your claim.

    I can print copies the first page of a recipe book over and over but have very little confidence this will produce a new recipe no matter how much deep time I have to do this.

  12. colewd: There are 200 unique proteins in the spliceosome.

    Unique in what sense?

    How would gene duplication account for these.

    That’s like asking “how does this process that accounts for these, account for these?”.

    A gene encoding a protein is duplicated, they diverge by mutations so there’s now two instead of one. And so on.

    Gene duplication followed by mutation would generally break down a sequence.

    That’s why the structure is so gratuitously complex. Have you heard of constructive neutral evolution?
    Read this: How a Neutral Evolutionary Ratchet Can Build Cellular Complexity.

  13. colewd:
    The existence of these paths is an evolutionist claim. There is no reason for them to exist and no experimental data showing they exist.
    [snip]
    I think you need to show that replication and variation can generate FI. So far the evidence does not favor your claim

    Sez you. To the Hayashi and Keefe & Szostak papers I cited earlier (and you studiously ignored, quelle surprise!) I should add pretty much the entirety of Joe Thornton’s career.
    You are claiming that replication and variation cannot generate [any?] FI, and that there are no accessible pathways from lower levels of function to higher levels, and most impressively you are claiming that the ‘evidence’ favors these claims.
    Are you going to make any attempt to support this claim by producing and discussing evidence, or can we expect a further round of unsupported assertions?
    Although I will give credit: you are at least explicit in your invoking of the “twas ever thus” fallacy. That’s honest, if clueless.

    [Off topic: I edited Rumraket’s post, thus committing a flagrant violation of the site rules]

  14. colewd: There is no real reason to believe that the ancestral state is different then it is today

    colewd: We are observing preserved sequences from species that split billions of years ago.

  15. Rumraket,

    That’s why the structure is so gratuitously complex. Have you heard of constructive neutral evolution?
    Read this: How a Neutral Evolutionary Ratchet Can Build Cellular Complexity.

    I had not heard of it but l looked over the paper briefly. Thanks for the citation.

  16. DNA_Jock: [Off topic: I edited Rumraket’s post, thus committing a flagrant violation of the site rules]

    Thank you for correcting the bad formatting. Posted and then went afk before checking 🙂

  17. DNA_Jock,

    Sez you. To the Hayashi and Keefe & Szostak papers I cited earlier (and you studiously ignored, quelle surprise!) I should add pretty much the entirety of Joe Thornton’s career.

    I have looked at this evidence. I am surprised that you think this solves the problem of supporting that evolution can create the FI we are observing.

    The paper that Rum cited attempts to explain how complexity arose like the spliceosome or the ribosome. What the paper is lacking is experimental evidence supporting the claim.

    Binding ATP or binding for transportation is just the beginning of trying to explain what we are observing.

    What you are choosing to ignore is that Hayashi could not demonstrate that mutation could find the function that was observed ie the wild type.

  18. colewd:
    I have looked at this evidence.I am surprised that you think this solves the problem of supporting that evolution can create the FI we are observing.

    I’m, however, not surprised that you don’t see how easy it is for evolutionary processes to produce information. It’s as if you had some deep reason to be unreasonably skeptical when it comes to something that conflicts with your beliefs, and unreasonably naive for things that agree with your beliefs.

    colewd:
    The paper that Rum cited attempts to explain how complexity arose like the spliceosome or the ribosome. What the paper is lacking is experimental evidence supporting the claim.

    The paper had plenty of evidence. You just might not have the background to understand it. However, the authors were very clear that this was just an exploration of one way in which complexity could arise. They were not affirming that’s how it happened. Yes. I know, why do I give you excuses, right? Well, it’s not that I’m giving you excuses, it’s that I evaluate things as presented, and for their actual goals. So, I would not try and sell you that as The Solution. That would be as dishonest as gpuccio pretending to pass a linear, direct, one-by-one mutation for the way a sequence could be mutationally saturated, just to avoid confronting the implication that if there was saturation, then evolutionary processes would have explored quite a bit of sequence space.

    I’d imagine that you still ignore this detail, since you think that gpuccio is measuring functional information when he compares sequences, yet you keep ignoring this implication. Why would you not care about this problem?

    colewd:
    Binding ATP or binding for transportation is just the beginning of trying to explain what we are observing.

    Yeah, and those bindings occur very easily in random peptides. Intelligent designers on the other hand, remain in the realm of the imaginary.

    colewd:
    What you are choosing to ignore is that Hayashi could not demonstrate that mutation could find the function that was observed ie the wild type.

    You are making several mistakes here. They did find sequences that performed the function. Only not at the level of the wild type. They didn’t talk about reaching the wild type, but for wild-type levels of activity. Those two things are different. In other words, they were not aiming for the same sequence, just for the same activity. If you keep ignoring that different sequences can perform the same activities you’ll continue ignoring why we’re not impressed by creationists talking about the probability of an extant sequence.

    Hayashi and friends were also talking about their set up, which lacks such phenomena as recombination, which is known to accelerate things quite a bit. Also, it’s not just mutation, it’s also selection.

  19. colewd: What you are choosing to ignore is that Hayashi could not demonstrate that mutation could find the function that was observed ie the wild type.

    No, I chose to discuss that. So did Entropy. You merely assert, without foundation.

  20. DNA_Jock,

    After thinking about this it appears you are committing the TSS fallacy as you are trying to define FI (generating the minimum selectable function) as something different then what we are observing which is FI that generates the wild type transporter.

    The whole idea of a minimum selectable function makes too many assumptions. One in the Hayashi case is the 300 non randomly generated AA’s that accompany the 130 randomly generated ones. It also takes for granted all the other sequences that are necessary for transport to occur.

    In gpuccio’s case we are observing FI that generated similar AA sequences despite a split over a billion years ago.

  21. colewd:
    DNA_Jock,
    After thinking about this it appears you are committing the TSS fallacy as you are trying to define FI (generating the minimum selectable function) as something different then what we are observing which is FI that generates the wild type transporter.

    That makes zero logical sense. One can’t be committing the texas sharpshooter fallacy by explicitly NOT picking out a particular target out of a potentially huge ensemble and NOT insisting this is the one that HAS to be hit.

    Look, evolution merely has to work with whatever function happens to exist in the sequences sampled, it doesn’t matter whether you think this is a high or low amount of FI. What matters is if it is enough to allow a lineage to avoid extinction.

    The function discovered by Hayashi et al clearly allows the phage to improve fitness and continue to exist, so that is all that matters. That’s what shows that as long the organism can persist and reproduce, evolution can change a nonfunctional sequence into a functional one.

    What this tells us is that there is a high enough frequency of a minimum selectable function in the sequence neighborhood of an arbitrary function to allow evolution to improve it through positive selection. And that’s not an assumption, that’s the result of the experiment.

    Remember, at the outset of the experiment the random protein domain from Hayashi et al had a comparable level of activity to a protein that had the entire domain deleted. So whatever that D2 domain from the wild-type g3p protein does, was not absolutely essential to the survival and existence of phage.

    The whole idea of a minimum selectable function makes too many assumptions.

    What assumptions are those? Spell them out.

    One in the Hayashi case is the 300 non randomly generated AA’s that accompany the 130 randomly generated ones.

    What about them? Is that an assumption? How? Spell out the issue.

    It also takes for granted all the other sequences that are necessary for transport to occur.

    Uhh yes, of course. There has to be a living organism that can function for an experiment in evolution to even be possible. They’re not conducting an experiment in the origins of life. Turning something dead into something alive.

    They’re conducting an experiment in the origins and improvement of a particular non-essential function for an organism.

    Obviously if the function has become essential to the organisms ability to even survive then it can’t be removed and then re-evolved. Nobody claims otherwise.

    The conclusion we can draw from this is that the wild-type D2 domain of the g3p protein has not become absolutely essential for the survival of phage. But it’s absence still results in a millionfold reduction in infectivity. That’s an enormous fitness loss. Even so, phage can apparently still persist without it, and a random protein in place of the D2 domain can evolve up a hill in the landscape and in a mere 20 generations improve infectivity seventeen thousand-fold.

    Add another 200 million generations and genetic recombination on top, what could then evolve?

    In gpuccio’s case we are observing FI that generated similar AA sequences despite a split over a billion years ago.

    Please elaborate on the particular case you’re thinking of here, not sure what thing you are referring to.

  22. colewd:
    After thinking about this it appears you are committing the TSS fallacy as you are trying to define FI (generating the minimum selectable function) as something different then what we are observing which is FI that generates the wild type transporter.

    I think that you don’t understand what the TSS fallacy is about. When you define FI as being just about the exact sequences we’re observing, that’s when you commit the TSS fallacy, since you draw your target circles around the observed sequence(s), and declare that to be the one and only target.

    Also, it’s not the information that generates a sequence, it’s the sequence that contains the information.

    colewd:
    The whole idea of a minimum selectable function makes too many assumptions.

    Assumptions? Like “this is the one and only sequence that could perform a function”? Like that assumption? The existence of minimally selectable functions has been tested several times in the laboratory, and the results are very promising. You prefer to be unreasonable skeptical about them, then you turn around and take anything, no matter how misinformed, from the ID camp, and accept it blindly.

    colewd:
    One in the Hayashi case is the 300 non randomly generated AA’s that accompany the 130 randomly generated ones. It also takes for granted all the other sequences that are necessary for transport to occur.

    You’re mistaking an experimental set up for an assumption. The experiment was set to test for the evolution of a peptide that could compensate for the lack of some specific activity, thus the set up. Different set ups test for different things. That’s not assumptions, that’s experimental design. The authors were not trying to produce a brand new life form.

    colewd:
    In gpuccio’s case we are observing FI that generated similar AA sequences despite a split over a billion years ago.

    Again too many things wrong with this sentence. As I said, it’s not the FI that generates the sequences, it’s the sequences that contain the FI. Your friend takes the measures of similarity to represent the amount of FI in the sequences. So this is about the amount of conservation of the sequences after separation, not about independently achieved similarity (but if you think it was independently generated, then you think that evolution has quite the capacities, which would be a tad contradictory to your preferred position). There’s many problems with using those measures of similarity to represent FI, but the one we’re discussing right now (or at least you and DNA_Jock), is that you’re taking the one and only sequence you observe to be the one and only that could have performed the function, which is, as DNA_Jock has tried to explain too many times, a TSS fallacy.

    Wanting evolution to be false won’t make it false. Being obtuse when it comes to evidence for evolution, while being excessively naive about misinformed arguments against it, won’t make evolution false either.

  23. colewd:
    There are 200 unique proteins in the spliceosome.How would gene duplication account for these.Gene duplication followed by mutation would generally break down a sequence.

    Which is what’s avoided by the selection pressures, not always successfully, which is why there’s plenty pf pseudogenes around the successful gene duplicates. Do you really think that scientists haven’t thought that mutations can break down sequences?

    colewd:
    All the systems I mentioned have more then 500k AA’s.We can quibble over how much FI that is but I think we can agree that it is more then 500 bits.

    And we’re supposed to be impressed by that?

    colewd:
    The design inference is based on the observation of FI in biology.

    Nope. The design inference is made out of wishful thinking, poor philosophy, poor scientific understanding, poor logic, and a religious commitment to prove the existence of some magical being in the sky.

    colewd:
    There is no real reason to believe that the ancestral state is different then it is today other then trying to make the simple to complex model work.

    Of course there’s plenty of reasons. The fossil record shows that, for example, eukaryotes have not existed all along, that life has been microbial for a very long time, that there’s been succession of life forms. The most ancient fossils seem to be similar to bacteria. Sequence analysis also tends to put lots of proteins into families, even many proteins that have diverged quite a bit and whose ancestral relationships are not that easy to establish, which means that such families started from one, to complexity coming from something simpler. There’s also the fact that we’re looking for answers, and, given what we know, it is not possible to life to have arisen as, say, humans sprouting out of nowhere in one go. It all points to simpler life forms in the earlier stages of life.

    colewd:
    If we look at the minimum requirement for life it includes cell division.This is a very precise and complex process which excludes the idea of a simple beginning.

    In which organisms? Cell division can be very simple. For example, micellar structures tend to divide in two and split their contents on their own after getting too big to remain being a single micelle. It’s with the evolution of more complex systems that the requirements for complex cell division evolve. It’s not an all or nothing thing. Simpler cells have simpler ways of dividing their cells. Obviously. So why would anybody ignore this and center on human cells unless they didn’t want to figure it out? Unless they didn’t want it to be figured out?

  24. Rumraket,

    That makes zero logical sense. One can’t be committing the texas sharpshooter fallacy by explicitly NOT picking out a particular target out of a potentially huge ensemble and NOT insisting this is the one that HAS to be hit.

    The fallacy is that he is arbitrarily adding a wider spread of bullet holes to the target. The minimum selectable function is not what we are observing and it is at best a theoretical construct. He is denying what is being observed. The texas sharp shooter fallacy can be either making the shooter look better then he actually is or worse then he actually is. Jocks fallacy is the latter.

    Look, evolution merely has to work with whatever function happens to exist in the sequences sampled, it doesn’t matter whether you think this is a high or low amount of FI. What matters is if it is enough to allow a lineage to avoid extinction.

    We may disagree but I think it takes at least 100k bits of FI for eukaryotic cell division. I am estimating at least 150 bits added per new protein. This information is an addition to what we are observing in prokaryotic cells. This is very strong support for the design inference if I am right.

    Add another 200 million generations and genetic recombination on top, what could then evolve?

    200 million generations is 2X10^8 generations. Hayashi claims 10^70 sequences in his library to find the wild type. This is a relatively simple living application. The function of genetic recombination and its role in living diversity is an interesting comment that Entropy also has been making.

    Please elaborate on the particular case you’re thinking of here, not sure what thing you are referring to.

    The beta chain of the F1 subunit of ATP synthase.

  25. dazz notes something strange:
    colewd: There is no real reason to believe that the ancestral state is different then it is today

    colewd: We are observing preserved sequences from species that split billions of years ago.

    Isn’t that odd? For millions of years huge amounts of functional information were being added (in large “information jumps” no less), yet there cannot have been simple precursor, because all the extant sequences are highly conserved and intolerant of mutation. So what exactly has been added? What is that mysterious “function”?

  26. colewd: We may disagree but I think it takes at least 100k bits of FI for eukaryotic cell division. I am estimating at least 150 bits added per new protein. This information is an addition to what we are observing in prokaryotic cells. This is very strong support for the design inference if I am right.

    My, what a precise quantification. Without doing any calculations whatsoever, I note. You mention 100k and 150 bits of functional information? Those certainly are big numbers with lotsa zeroes. But could you specify what function, please? Hint: “eukaryotic cell division” is not the function you are discussing, because what you really mean is “MODERN eukaryotic cell division”, with which you really, really mean MODERN HUMAN eukaryotic cell division. And if you want to argue for that, then you need to make a plausible case that cell division in the first eukaryotic ancestor was precisely as observed in modern humans (which it wasn’t), show how it is different from prokaryotic cell division, and demonstrate that the former cannot possibly have evolved from the latter. You have made no attempt at any of those.

    Please note: Under your current definition, absolutely *zero* functional information has been added since the first eukaryote, because human cells are capable of division, just like our ancestor was 2 billion years ago, at the same level of efficiency as far as we can tell.

    So be precise. What aspect of eukaryotic cell division is impossible to evolve, according to you?

  27. colewd: The fallacy is that he is arbitrarily adding a wider spread of bullet holes to the target. The minimum selectable function is not what we are observing and it is at best a theoretical construct. He is denying what is being observed. The texas sharp shooter fallacy can be either making the shooter look better then he actually is or worse then he actually is. Jocks fallacy is the latter.

    No Jock, It’s YOU that is doing the sharp shooting! Painting the whole side of the barn when it is plain as day what the shooter was aiming for!

    IDers and analogies, love it 🙂

  28. colewd: The fallacy is that he is arbitrarily adding a wider spread of bullet holes to the target. The minimum selectable function is not what we are observing and it is at best a theoretical construct. He is denying what is being observed. The texas sharp shooter fallacy can be either making the shooter look better then he actually is or worse then he actually is. Jocks fallacy is the latter.

    That’s really funny. I am not adding a wider spread of bullet holes, nor am I making the shooter look worse than he actually is. The bullet holes are the bullet holes. They may be tightly grouped (which is indicative of a consistent shooter) or not. I am not changing any bullet holes; I am merely pointing out that the target is bigger (much bigger) than gpuccio’s lame-ass post-hoc paint job.
    What Corneel said about analogies.

  29. DNA_Jock,

    I am not changing any bullet holes; I am merely pointing out that the target is bigger (much bigger) than gpuccio’s lame-ass post-hoc paint job.
    What Corneel said about analogies.

    Sure you are. Gpuccio is comparing actual sequences. Your claim that the target is much bigger is texas sharp shooting speculation. You are claiming a larger target shy of evidence of its existence.

  30. Corneel,

    But could you specify what function, please? Hint: “eukaryotic cell division” is not the function you are discussing, because what you really mean is “MODERN eukaryotic cell division”, with which you really, really mean MODERN HUMAN eukaryotic cell division.

    Is this an attempt at a sharp shooting fallacy:-)

  31. Corneel,

    Isn’t that odd? For millions of years huge amounts of functional information were being added (in large “information jumps” no less), yet there cannot have been simple precursor, because all the extant sequences are highly conserved and intolerant of mutation. So what exactly has been added? What is that mysterious “function”?

    Yes. It is hard to explain the data without speculation except with the design inference. The evidence is very strong that these sequences don’t have a random origin.

  32. colewd:
    The evidence is very strong that these sequences don’t have a random origin.

    Of curse they don’t have random origins. They contain an accumulated history of successful selection imprinted all over them. Selection is not random. Natural phenomena, while containing random elements, are not random. If they were random we’d just check the distribution they follow and be done with it.

    The question is not whether they arose randomly or not, but about the processes and the history behind them. You prefer not to ask these questions, but, instead, to affirm that god-did-it. I prefer to try and actually figure things out. To each their own.

    Seems like we’re not in talking term any more. That’s all right. I just didn’t get the memo.

  33. Entropy,

    Seems like we’re not in talking term any more. That’s all right. I just didn’t get the memo.

    Were fine. I am just thinking about your comments before responding as they have some new ideas. It has been a while since we have exchanged.

    The question is not whether they arose randomly or not, but about the processes and the history behind them. You prefer not to ask these questions, but, instead, to affirm that god-did-it. I prefer to try and actually figure things out. To each their own.

    I also prefer to figure things out but what is the best current explanation we have? Design does not point directly to God but points in His direction. What we are observing is almost certainly deterministic. Could genetic recombination be a deterministic process that accounts for the diversity we are seeing. Perhaps.

  34. colewd:
    Were fine.I am just thinking about your comments before responding as they have some new ideas.

    That’s really nice of you.

    colewd:
    It has been a while since we have exchanged.

    Yeah. I’ve been very busy.

    colewd:
    I also prefer to figure things out but what is the best current explanation we have?

    Depends on what you call “explanation.” If we define explanation as something whose workings can be understood, then the best explanation is that the way nature works leads irremediably to life having no option but to evolve.

    colewd:
    Design does not point directly to God but points in His direction.

    I’d think that design points to us. So far I haven’t seen any design that wasn’t made by humans. It depends on what we call design though. Other definitions would add what some other life forms do. Yet other definitions would include the products of geochemical processes. But let’s not go there.

    colewd:
    What we are observing is almost certainly deterministic.

    If so, then talking about randomness would be somewhat meaningless. Right? If determinism is part and parcel with nature, then talking about whether it’s design or random would be nonsense (it is still nonsense, a false dichotomy, since we know that at least some natural processes are deterministic, but if we go all the way to abject determinism, it gets much more evidently nonsensical, right?).

    colewd:
    Could genetic recombination be a deterministic process that accounts for the diversity we are seeing. Perhaps.

    Interesting thought. As far as I understand, recombination is one of the processes though. Not the only one.

    Please keep thinking. No rush. Also, I’ll be again extra busy the next few weeks. So I might not be able to give you a lot of answers.

  35. colewd: Could genetic recombination be a deterministic process that accounts for the diversity we are seeing. Perhaps.

    No perhaps about it. Genetic recombination cannot explain the great majority of differences among species. A look at any set of DNA sequences will show you that. There must be mutations, and some of those mutations must eventually become fixed in different lineages.

  36. colewd: Is this an attempt at a sharp shooting fallacy:-)

    It is an attempt to get you to be explicit about the function of the 100,000 bits of Functional Information in eukaryotic cell division, instead of leaving it hanging in the air. If you are able to put a number to it, we should be able to quantify it somehow right?

    colewd: Yes. It is hard to explain the data without speculation except with the design inference. The evidence is very strong that these sequences don’t have a random origin.

    But but but, I was trying to use the design inference. That is what led to my confusion: How can genomic sequences accumulate enormous amounts of functional information (a measure of system complexity), but simultaneously not be an example of a simple to complex model?

    Also: the only reason the design inference is free from speculation is because we are explicitely forbidden to do so, until we have swallowed that organisms are designed.

  37. Corneel,

    It is an attempt to get you to be explicit about the function of the 100,000 bits of Functional Information in eukaryotic cell division, instead of leaving it hanging in the air. If you are able to put a number to it, we should be able to quantify it somehow right?

    The 100k bits is very conservative. If we look at PRP8 which gpuccio estimated at 2500 bits is one of several thousand proteins that are necessary for the transition. I think there is an argument for over 1 million bits so 100k should be a reasonable number.

    How can genomic sequences accumulate enormous amounts of functional information (a measure of system complexity), but simultaneously not be an example of a simple to complex model?

    This is a good point but we have no evidence of simple life. The better way to state it is complex to increased complexity.

    Also: the only reason the design inference is free from speculation is because we are explicitely forbidden to do so, until we have swallowed that organisms are designed.

    I think the design inference has its weakness as it only explains by human analogy. On the other hand it is the only way we have seen FI generated with the possible exception of genetic recombination which Harshman believes is only a partial explanation. GR may also only be re arranging existing information.

    For FI you need a purely deterministic process IMO where if trial and error is involved conscious revisions are made as a result of analyzing the error. You can use an algorithm but the end sequence must be known if the sequence is of any appreciable length.

    I don’t think gpuccio’s analysis is perfect but it is the beginning of a real study of life’s diversity. The origin and ever increasing infusion of FI. Where does the FI come from? Where do atoms come from:-)

  38. colewd: On the other hand it is the only way we have seen FI generated with the possible exception of genetic recombination which Harshman believes is only a partial explanation. GR may also only be re arranging existing information.

    Given that you have no definition of information and no way to determine whether a given change increases is there’s really no way you can make such an asswertion. And let me suggest that recombination can be only a very minor component. It’s overwhelmingly mutations that change sequences. I’m also not sure what you think “recombination” means.

  39. colewd: The 100k bits is very conservative. If we look at PRP8 which gpuccio estimated at 2500 bits is one of several thousand proteins that are necessary for the transition. I think there is an argument for over 1 million bits so 100k should be a reasonable number.

    Impressive. Truly impressive. If I understand you correctly, the following is true, per Cole-Puccio math:

    I discover a previously uncharacterized protein, PRPX. Although it bears detectable homology to PRP8, it performs a distinct function, and is necessary for eukaryotic cell division. gpuccio reviews the sequences of identified homologs across phyla and concludes that PRPX contains 1,661 bits of FI. Hey, it’s sequence isn’t as tightly conserved as PRP8.
    Because PRPX is essential (today) and it has 1,661 bits of FI, the existence of PRPX makes the unguided evolution of eukaryotes 10^500 times less likely than previously thought.
    Two such proteins would make evolution 10^1000 times less likely.

    And you are okay with this calculation? It doesn’t strike you as a little whacked that this one protein has such a whopping effect on your probability calculation?
    I mean, the difference between your 100k bits (conservative) and 1 million bits (what you really think) is a ten-to-the-270,000 fold difference. That’s quite the margin of error. You think you are being 10^270,000-fold conservative; I mean, I appreciate your generosity here, but aren’t you just a tad concerned that your results make no sense?.
    Do you understand exponents?
    [Hint: in addition to TSS etc, you are also committing the fallacy of assuming independence]

  40. John Harshman,

    Given that you have no definition of information and no way to determine whether a given change increases is there’s really no way you can make such an asswertion.

    The Szostak/Hazen paper is the definition being used in this op. If you study the Hayashi paper it will give you strong evidence that random mutation is not a viable path to the FI we observe in nature.

    It’s overwhelmingly mutations that change sequences. I’m also not sure what you think “recombination” means.

    Yes, mutations do change sequences but this tells very little about the origin of the FI we are observing in nature.

  41. DNA_Jock,

    And you are okay with this calculation? It doesn’t strike you as a little whacked that this one protein has such a whopping effect on your probability calculation?

    All I see is your continued attempt to create strawman arguments and mislabel other arguments as fallacies. I don’t think gpuccio’s calculation is perfect but it is a viable way to estimate FI.

    The method looks at a protein observed in nature that exists in animals separated by hundreds of millions of years. It calculates the sequences that were preserved as evidenced by identities in both species. The protein performs the same function in both animals. That is the method.

    Although it bears detectable homology to PRP8,

    What is your method of detecting homology?

    Do you understand exponents?

    I understand them well enough to know that to make a claim over 100k bits of information is unnecessary.

  42. colewd: What is your method of detecting homology?

    pblast

    DNA_Jock: Because PRPX is essential (today) and it has 1,661 bits of FI, the existence of PRPX makes the unguided evolution of eukaryotes 10^500 times less likely than previously thought.

    You did not answer my question, to wit, are you okay with this calculation? I am not trying to strawman Cole-Puccio math. I believe that this is an accurate reflection of your calculations. If it is not, you need to explain, very precisely, just why it is not.

  43. colewd:
    John Harshman,

    The Szostak/Hazen paper is the definition being used in this op.If you study the Hayashi paper it will give you strong evidence that random mutation is not a viable path to the FI we observe in nature.

    By that definition, it’s impossible for the amount of information in a particular gene to change, isn’t it? I think you are misunderstanding the Hayashi paper.

    Yes, mutations do change sequences but this tells very little about the origin of the FI we are observing in nature.

    Yes, that’s because the definition you are using means that mutation can’t alter the amount of information.

    I’m still not sure what you think “recombination” means or why you brought it up.

  44. I am back after running a week-long workshop in a scenic place, which required a lot of work.

    Texas sharpshooting aside, I wanted to summarize my conclusions about gpuccio’s argument. First, he has no formal argument that 500 bits if functional information cannot be built into the genome by natural processes that include natural selection. He agrees that he does not have it, and instead regards it as an “empirical” conclusion.

    The 500-bit figure is supposed to rule out mutation alone as capable of building that much FI into the genome. I agree, it is a conservative figure for that. But it does not rule out natural selection, which can do the job if there is a path of increasing fitnesses into the set of sequences whose fitnesses are above the threshold.

    Instead of trying for a proof gpuccio asks whether you have a proof that it is possible. I think the shoe is on the other foot — gpuccio has to provide an impossibility proof. Without it we cannot be confident in our conclusion that such paths are ruled out.

    Conclusion: The 500-Bit Theorem does not exist.

    (More on the other two points in my OP later).

  45. colewd: The fallacy is that he is arbitrarily adding a wider spread of bullet holes to the target.

    No he isn’t. He’s simply pointing out that there are other ways to get the function in question performed by the D2 domain of the g3p protein from phage. That’s neither wrong, nor a fallacy.

    The minimum selectable function is not what we are observing

    Duh, it’s not like phage was magicked into existence yesterday. The protein we are seeing has evolved literally for tens of millions of years. It would have been a miracle if it had stayed at the level of minimally selectable function.

    and it is at best a theoretical construct.

    No, that is an unavoidable physical reality. There can’t not be such a thing as a minimally selectable function. It is the lowest level of function that natural selection can maintain. There simply has to be such a thing for any putative function performed by a system in a living organism. Take sight, the sense you use to see. It has a minimally selectable function. There is some point at which the sense of sight becomes so bad that it no longer aids in survival and reproduction. It’s probably pretty close to complete blindness.

    Or how about moving around? Locomotion. A human being will die if it is unable to move (or have protection from other humans that can). There is a minimum selectable amount of locomotion necessary to survive. So you can gather food and avoid predators.

    He is denying what is being observed.

    Not at all, he’s just explaining to you that all results are contingent on historical developments, and that you can’t pick out a particular one and insist that because that particular one is rare out of the ensemble of all possible functions, therefore it must have been picked out by a designer. That kind of ad-hoc reasoning will work for anything, as you can paint a circle around anything that evolves. He’s simply explaining to you how your reasoning commits the TSS.

    200 million generations is 2X10^8 generations.

    And if 20 generations can improve infectivity by a factor of 17000, what can another 200 million?

    Hayashi claims 10^70 sequences in his library to find the wild type.

    from the position in sequence space where they started the experiment, according to an extrapolation based on the assumption that the global landscape is correctly described by what they call the n-k model. I don’t see you questioning or even wondering about the assumption, or the extrapolation. You seem to be focused intensely on The Big Number though. You had complaints about “assumptions” in a previous post that you failed to elaborate on, but if those assumptions can be interpreted to lend support to a design argument from Big Numbers(tm) those assumptions must be absolutely correct.

    Ironically, the n-k model is actually a theoretical construct, and the model used to determine what constitutes the minimally selectable function for the RP3-42 protein. You reject the concept of a minimally selectable function based on the n-k model, but you’re fine with an extrapolation into the unknown based on that very same model and it’s assumptions, simply because you think you can construe the Big Number it yields as lending support to a design-inference.

    Either you simply don’t understand what is going on here, or you have a double standard. Or both.

    This is a relatively simple living application. The function of genetic recombination and its role in living diversity is an interesting comment that Entropy also has been making.

    What does “interesting” mean here? That you concede that it is possible that recombination significantly increases the likelihood of blind exploration of sequence space to find levels of activity similar to the wildtype? Then you can’t infer design from the existence of the wildtype, as Cole-Puccio math hasn’t accounted for such a scenario.

    The beta chain of the F1 subunit of ATP synthase.

    Yeah, that one is relatively conserved for the function of ATP hydrolysis or synthesis. But there are many variants of that protein that perform other functions. Again, the P-loop containing kinases (of which ATP synthase/ATPase is just one variant) is a huge superfamily of related proteins that perform hundreds of different biochemical functions in life. They are wildly divergent. So while a rough overall structure has been conserved across the diversity of life, the sequences are very divergent. It is simply wrong to insist the protein can’t mutate, it just that among those mutations are ones that cause it to takes on other functions than ATP synthesis and hydrolysis.

    You can’t just look at the subunit in ATP synthase to see how divergent those are, when there are many other proteins with the same fold, at much larger degrees of sequence divergence that perform other functions (some functions more similar, others less so).

  46. colewd: The evidence is very strong that these sequences don’t have a random origin.

    There is zero evidence for that. What evolves is largely contingent on what sequence the protein originally evolved from. It could be relatively closeby in sequence space. As I tried to get you to understand with that drawing multiple times.

    You can’t just rule out that the wild-type evolved from another location much closer to the local hill it sits on. Couching your claim that this couldn’t happen in terms of “Functional Information” does not accomplish that either. That’s just fancy window dressing for an argument based on the same basic fallacy.

  47. Joe Felsenstein,

    Instead of trying for a proof gpuccio asks whether you have a proof that it is possible. I think the shoe is on the other foot — gpuccio has to provide an impossibility proof. Without it we cannot be confident in our conclusion that such paths are ruled out.

    This point is nonsense.

    Here is my hypothesis (natural selection) and unless you can prove that it is impossible it stands as the hypothesis of record.

    He is saying with 500 bits he can safely infer design. This is an inference and you are having to create a strawman called an “impossibility proof” to defeat his argument.

    The question is not whether one side is impossible it is which explanation best fits the observation of 500 bits of FI.

    His point is that you lack evidence that there is a large enough quantity of selectable sequences inside the proteins we are observing for a realistic selectable path to the observed sequence. Without an enormous amount of selectable sequences natural selection is not a viable explanation for the current observed FI in nature.

    At the end of the day your claim is that 500 bits of information do not exist in nature because if there is a selectable path and 500 bits is impossible to navigate through then the existence of a selectable path says there is less than 500 bits in the sequence.

    When Darwin constructed this theory he had no idea that he had to find functions through large sequences.

  48. Rumraket,

    You can’t just rule out that the wild-type evolved from another location much closer to the local hill it sits on.

    I think we can rule it out as a viable mechanism. You are struggling to make your point with the simplest life forms.

  49. John Harshman,

    By that definition, it’s impossible for the amount of information in a particular gene to change, isn’t it? I think you are misunderstanding the Hayashi paper.

    No. Loss of information is quite easy to explain. Gain is another challenge.

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