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 
. 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?
And all it took was purifying selection to keep it highly functional along the way. That shit doesn’t in anyway, shape or form lend support to any design hypothesis, and you basically conceded darwinian mechanisms can account for all evolution since the LCA of E Coli and humans as far as the beta chain goes. Way to shoot yourself in the foot, dummy
Corneel,
No. Not sure how you got here>
For one thing, because that is how our friend gpuccio explained the absence of TRIM62 in cnidaria:
… which suggests a specific molecular function in humans, no? And also because you mentioned “a specific function of two or more different animals”. But I confess that I do not fully grasp what you mean, as you guys leave me doing a lot of guesswork here.
Perhaps you could give an example of a specific function and tell me how this is different from the it-works-or-it-is-broke function that we observe in human engineered parts?
I’ve been trying to explain that contradiction to them, but they seem unable to grasp it.
Corneel,
No, it suggests the origin of the function was in vertebrates.
We expect a eukaryotic vertebrate cells to divide rapidly during embryo development and then slow down as the animal matures. One of the ubiquitin regulation genes is the APC gene/protein which binds to beta catenin and is involved in the destruction process. If there is some key mutations of this gene binding fails and cell division loses control. This greatly increases the risk of certain cancer types. This process involves many proteins and is very sensitive to mutation.
Joe:
colewd:
That made me laugh.
Bill, you are completely lost. As usual.
A function that wasn’t there before but is now required in all extant vertebrates, including humans, right?
So if there are mutations in the gene for adenomatous polyposis coli protein (APC), it fails to correctly antagonize the WNT signalling pathway, leading to an increased risk of colorectal tumor. A perfect example of a binary all-or-none function, is it not?
Look, it is clear that you cannot explain how this “specified function” qualifier makes a iota of difference to Joe’s appraisal of your position. It is obvious that you are taking “function” to either exist or not, and are taking the threshold as set properly when it manages to separates sequences that are functionial from the ones that are not. This is clear from the two examples you gave above, and is a logical consequence of viewing organisms as being designed: If any of the parts break, they will malfunction, like clockwork soldiers.
I just don’t understand why you insisted on this empty tack-on of “specified function”. It is completely superfluous, so why is it so important to you?
None of which says the system couldn’t evolve, or continue to evolve. Just that among the possible mutations in the genes that make up this system, some will be deleterious or lethal.
If you wish to extend this statement to conclude that the system couldn’t have evovled to begin with, nor have diversified in vertebrates, nor continue to evolve into the future, then you’re stuck in black and white/all-or-nothing thinking again.
Corneel,
Do you think that the APC gene/protein or the WNT pathway don’t have a specified function in the cell?
Rumraket,
Exactly. It can evolve loss of cell cycle control:-)
LOL! The very reason I have been pressing you on this is because I have no clue what you mean by that.
Do you know what Wnt stands for? It is a mash of Wingless (Wg) and integration1 (int1). The Wingless gene was identified in Drosophila as a mutant giving rise to incorrect wing development, and it was later found to be an important determinant of segment polarity during fruitfly development. The homologous int1 gene was later identified as a proto-oncogene in mice, and regulates cell proliferation and migration. The pathway is involved in many other biological functions as well. There have been some crazy design decisions there (can you say co-option?).
So please go right ahead and tell me: What IS the specified function of the Wnt pathway in the cell? I am all ears.
But all that is besides the point. The question I am trying to get you to answer for some time now is: If the specified function of a protein is the only function it can perform (the function it was designed to do, I suppose), then what is the point of distinguishing between specified function and plain vanilla function? Especially since you guys never bother to specify any function anyway.
Sounds like it could have been designed better to me.
Corneel,
Cell cycle control both in embryo development and mature animals. The ubiquitin system operates inside this pathway.
Corneel,
It can have multiple specified functions:-)
For example?
How do you know? Perhaps it’s for something entirely different.
After all, it could can have multiple specified functions:-)
OMagain,
If you do a pubmed search you will see 20000 hits for the WNT pathway as it is implied in most cancers when it loses regulation. One of its major roles is cell cycle control.
Of course.
OMagain,
Cytochrome c is part of electron transport and apoptosis two very different functions.
I do not think that covers it: I already told you that Wingless is a segment polarity gene. Why isn’t that part of its specified function? (other than that humans do not have segments, I mean)
So it is nonfunctional outside of animals?
Corneel,
So are you claiming that segment polarity is not part of cell cycle control?
Watch it. Your anthropocentrism is showing, Bill 😉
Corneel,
Huh?
And perhaps that is a secondary function. Or perhaps that function is just a by-product of it’s actual specified function.
You simply don’t know.
Those are two functions. Who or what specified them?
That is correct, Sir. Determining segment polarity is part of the developmental program in animals that have segments, like insects.
Corneel,
So are you claiming that animal develop without triggering the cell cycle?
Apoptosis occurs in multicellular organisms, usually in the context of animal development
I’m interested to know what the specified function of a segment polarity gene is in humans, who don’t have segments. Your question is an obvious attempt at obfuscation.
OMagain,
Yes, we do know. Cell division in not a sideshow of biology it is one of its most distinguishing functions.
OMagain,
Are you claiming humans are single cell organisms? Now that would get peoples attention:-)
I am claiming that the (hem hem) specified function of the members of the Wnt signaling pathway goes beyond cell cycle control, as demonstrated by the role of Wingless as a morphogen during insect development.
What’s the problem? I thought that proteins could have multiple specified functions?
Corneel,
J Exp Bot. 2008;59(3):435-44. doi: 10.1093/jxb/erm258. Epub 2008 Feb 5.
Programmed cell death in plants: distinguishing between different modes.
Reape TJ1, Molony EM, McCabe PF.
Corneel,
Not a problem and not part of the argument I am just trying to sync up on the facts. Cell cycle control is a very complex function with many sub functions under it. WNT involves hundreds if not thousands of proteins.
Out of interest, could you write out in your own words the question you think you answered with that comment?
The specified function of a jeep is to carry passangers. Yet to lions its purpose is to provide them with some handy shade in the hottest part of the day.
It’s function changes depending on who you ask. I’m just interested to know who you think is setting the specifications?
What’s it’s function then?
Oh, well done. Now for some unicellular organism, please (they have cytochrome c too).
OMagain,
Yet if we talk about its engine or its wheels the function narrows.
Corneel,
Do I win a warm ale yet:-)
Quite. That’s why I would like to hear precisely what molecular or biological function we are discussing, instead of some vague handwaving. I also hope that, given the many tasks that Wnt signaling takes care of, you appreciate now that co-option of existing molecular function (like signaling pathways) is a pretty darn good contestant for increasing biological complexity.
Haha, absolutely.
Corneel,
Co-option. Like borrowing a bike tire when your car tire blows up?
Very interesting.
So, if I understand correctly, cyt c has multiple (specified by colewd) functions, including electron transport and apoptosis.
When gpuccio does his FI-related calculation, he chooses a function and determines how much FI* the protein has. Say he picks electron transport. Let’s further suppose (counter-factually) that he is able to accurately calculate the proportion of sequences that are capable of performing electron transport at a minimally selectable level. Electron transport is pretty much ubiquitous and pretty much ubiquitously essential, so gpuccio is pleased with the number of bits he comes up with.
Unfortunately (for Cole-Puccio math, that is) he has missed the “very different” specified function, apoptosis. Apoptosis is pretty much ubiquitous (in eukaryotes) but optional. So the minimal selectable function could be insanely broad-based. Shit, all of a sudden cyt c has only 10 bits of FI if you use apoptosis as the specified function.
Not that I think for a minute that this is how cyt c evolved; my point is merely that practitioners of Cole-Puccio math need to be able to identify and calculate the FI for minimally selectable levels of activity for all potential paths to the observed protein, not just the specified function that first grabs their fancy. [Joe F and others have made this point previously, but now colewd has explicitly noted the possibility of multiple (specified?) functions for a single protein.]
*that’s gpuccio-FI, not Hazen-Szostak-FI
DNA_Jock,
Can you show us a calculation using your minimum selectable function strategy? We might find it agrees with gpuccio’s method.
Gpuccio has a calculation for FI which is indirect. It is possible that he could get a very low bit count for cytochrome c using that calculation. So what?
DNA_Jock,
I have to admire your willingness to stretch an argument:-)
When the apoptosis function was removed from cytochrome c in a mouse embryo from a single mutation it formed without a forehead.
I don’t see how this will help, but here goes: 99.8% of sequences in the space have no effect on apoptosis. 0.1% have an adaptive effect. Minus logbase2(1/1000) = 10
Oh-err. Penny not dropped yet.
If there are multiple different specifications that produce multiple different FI values for a given protein, gpuccio has to use the lowest FI score obtained. Additionally, he needs to demonstrate that he’s done the calculation for all relevant functions. Tricky. Otherwise he would be guilty of …. you guessed it.
😉
How mammalocentric of you. We were talking about eukaryotes, Bill; did you not bother to look at the link I provided?
DNA_Jock,
Since cytochrome c has very little sequence conservation across living organisms gpuccio will also get a low bit score. Lots of different workable solutions seems to correlate with low sequence preservation.
Enough that he has captured most the variation. Statistical samples and such.
DNA_Jock,
I did. Does it cover embryo development?