Glancing at Uncommon Descent (I still do as Denyse O’Leary often reports on interesting science articles, as here*, and the odd comment thread can still provide entertainment), I see an OP authored by gpuccio (an Italian medical doctor) entitled The Ubiquitin System: Functional Complexity and Semiosis joined together, telling the story of the ubiquitin protein and its central role in eukaryote biochemistry in some considerable detail. The subtext is that ubiquitin’s role is so widespread and diverse and conserved across all (so far known) eukaryotes, that it defies an evolutionary explanation. This appears to be yet another god-of-the-gaps argument. Who can explain ubiquitin? Take that, evolutionists! I’m not familiar with the ubiquitin system and thank gpuccio for his article (though I did note some similarities to the Wikipedia entry.
In the discussion that follows, gpuccio and others note the lack of response from ID skeptics. Gpuccio remarks:
OK, our interlocutors, as usual, are nowhere to be seen, but at least I have some true friends!
and later:
And contributions from the other side? OK, let’s me count them… Zero?
Well, I can think of a few reasons why the comment thread lacks representatives from “the other side” (presumably those who are in general agreement with mainstream evolutionary biology).
- In a sense, there’s little in gpuccio’s opening post to argue over. It’s a description of a biochemical system first elucidated in the late seventies and into the early eighties. The pioneering work was done by Aaron Ciechanover, Avram Hershko, Irwin Rose (later to win the Nobel prize for chemistry, credited with “the discovery of ubiquitin-mediated protein degradation”, all mainstream scientists.
- Gpuccio hints at the complexity of the system and the “semiotic” aspects. It seems like another god-of-the-gaps argument. Wow, look at the complexity! How could this possibly have evolved! Therefore ID! What might get the attention of science is some theory or hypothesis that could be an alternative, testable explanation for the ubiquitin system. That is not to be found in gpuccio’s OP or subsequent comments.
- Uncommon Descent has an unenviable history on treatment of ID skeptics and their comments. Those who are still able to comment at UD risk the hard work involved in preparing a substantive comment being wasted as comments may never appear or are subsequently deleted and accounts arbitrarily closed.
I’m sure others can add to the list. So I’d like to suggest to gpuccio that he should bring his ideas here if he would like them challenged. If he likes, he can repost his article as an OP here. I guarantee that he (and any other UD regulars who’d like to join in) will be able to participate here without fear of material being deleted or comment privileges being arbitrarily suspended.
Come on, gpuccio. What have you got to lose?
It’s interesting that I ended a comment about gpuccio’s semantic games with this:
Guess what he did in response to this? Yep. he evaded the point by focusing on semantic details. Take a look yourselves.
Now his “answers”:
Sorry, sorry, what was that again?
So, of course not, but yes! He concludes that there’s increases in information. Oh, ah! No! Because I didn’t say “Simon says!” It doesn’t matter gpuccio. Focus. Otherwise you’ll never know why you’re so wrong. (Maybe it’s just that gpuccio doesn’t want to know if he’s wrong. Maybe he feels that he has to be right no matter what.)
I never said “generic” either.
I understand them all right. You seem to be the one trying very hard to miss each and every point. Not my fault if this is too hard for you and your ego.
Gpuccio doesn’t seem to get that rather than the protein being conserved over the history of life, it has diversified into many new functions.
I think he wants to imply that if you change the protein too much, it stops working as an ATP synthase, which would then imply it is a much tinier “target” in sequence space(thus, again, committing the TSS fallacy).
But what has happened is the protein has changed a lot but took on new different functions instead of becoming nonfunctional. ATP synthase/ATPase might not even be the ancestral function of the whole P-loop NTPase superfamily.
Of course, another problem with his thinking is when he just assumes the protein had to somehow pop up de novo and couldn’t have evolved from some ancestral sequence incrementally.
It’s the usual gap-rationalizations creationists also employ wrt fossils. “Where are the transitional forms?” Well, there are a few, and then we show sequences with varying degrees of divergence from ATP synthase. From say 60% similar to 30% similar to 20% similar to 10% similar.
“Oh but now there are more gaps, between the 60% to 30%, from 30% to 20%, and from 20% to 10%. So they must be entirely different proteins created de novo.” One cannot facepalm enough at this kind of infinite moving of goalposts.
Because there is some “gap” in sequence between the many different forms of the P-loop NTPase superfamily proteins, he thinks these gaps couldn’t possibly have been traversed. He doesn’t understand that we are looking at the result of a historical process that inexorably yields divergence unless there is an almost omnipotent level of purifying selection. The ancestral versions were not retained, they changed and became the proteins we see today.
Of course there is some relationship between sequence and function, but rather than nonfunctionality, divergence in sequence in the case of the P-loop NTPase superfamily has allowed the protein to take on many different functions.
And I explained to you that gpuccio has several nested “arguments,” and that taking about one doesn’t mean that the other is not there, even if only implicitly. He defended all of the positions I mentioned in his new OP.
Which claim Bill? I explained to you the problem. Here it goes again: gpuccio “justifies” his “jumps” in “information” by saying that there’s been enough time for all the non-important sites in the sequence to have been “eroded” by sequence divergence. Do you get what that means? Read carefully: he’s saying that in “400 million years,” there’s been enough mutations that surely only the “functionally” important sites have been conserved (I’m using quotations because he’s surely going to say he never said “functional,” or he never said “information,” or he never said “jumps”). Got it? Enough time that all mutations that would change unimportant amino-acids would have already happened. Do you get it? Again, enough time that all mutations that would change unimportant sites would have happened. Clear? OK, what do you think that means? Given what it means, what do you think that means in terms of exploring sequence space? I’ll let you try and reach the conclusion that you seem to be avoiding. Please give it an honest try. Here, gpuccio is shooting himself in the foot.
Not according to my understanding of the relationship between energy and information. Not according to my understanding of evolution, not according to gpuccio’s shooting himself in the foot.
Gpuccip’s “discussion” is but hand waving, and a demonstration that he is really committed to the problem I mentioned and that you called a straw-man. The authors let a piece of protein evolve into increasing the phage’s infectivity. they succeeded in finding a peptide that increased infectivity by a lot. Gpuccio dismisses the work on two “grounds”:
1. That the infectivity didn’t reach what the wild type phage does.
2. That the sequence of the peptide was not similar to the wild type domain.
My take is different.
1. They succeeded in evolving increased infectivity using random peptides. Thus showing that evolutionary processes work. I didn’t expect perfection, since their tests are limited by the experimental design.
2. I expected that their evolved peptide wouldn’t look like the wild type domain. How so? Because, as I have insisted, there’s more than one way of attaining functions, so focusing on what’s already there doesn’t mean that no other solutions exist. Also, well, because if we start with random sequences, the probability of finding the very same solution should be slim.
Do you see how gpuccio’s second complain shows that he thinks that only the sequences that exist could perform the work? Now, again, what straw-man did I build?
I hope you read this carefully.
P.S. I found an article about an evolved peptide by the author mentioned, but I’m not sure it’s the same article, because the quotation gpuccio presents is not in the paper I found.
P.S. P.S. I think I found the right paper. 2006 it seems, PLoS ONE
Why would the random peptide in the Hayashi et al experiment just so happen to be able to help increase infectivity?
If the infectivity function is so exceptionally rare in sequence space that a “blind search” could not be expected to find it in the history of the universe, then why did a random peptide nevertheless turn out to have that exact functional capability? Should it not simply have had no effect until quintillions and quintillions of sequences had been probed?
Why was there functional versions even among the very first pool of random polymers used to start the experiment? THEY USED TEN. TEN (10) random polymers to start the experiment with. Among those ten polymers, one had measurably higher levels of infectivity than the others. That meanst at least one of those then polymers had the desired function.
How is that possible if the function is “virtually impossible” to find by blind searching through mutation and selection?
Could it be that those kinds of functions are actually very frequent in sequence space, and just a few rounds of selection can have dramatic effects on the level of infectivity? Could it be that, essentially, it is just about increasing persistent low levels of binding-activity between amino acid side-chains? That, in fact, there is always some low level of binding activity going on between different molecules, and selection merely has to enhance this function by retaining mutants that bind stronger?
Also, isn’t it rather obvious that the random peptide used to replace the D2 domain constitutes either an entirely different hill from the wild-type D2 domain, in the fitness landscape of infectivity-conferring protein domains, or at least that it sits at position of local optima in a rugged landscape?
It is possible that the “hill” in the fitness landscape of proteins that have the same function as the wild-type D2 domain, is so broad, that a protein on one side of the hill will have so low levels of similarity to a protein on the opposite side of the hill, that they will not be detected as adopting similar structures at the sequence similarity level.
For those same reasons, the area in sequence space from where the “search” begins can have dramatic effects on the level of infectivity that is achievable with the ranges of population size and number of generations of mutation+selection used to run the experiment.
Wild-type levels of infectivity might be reachable from the opposite side of the hill. Not that the LEVEL of infectivity is even relevant here. IDcreationists are still left having to explain why the random peptide EVEN DOES help raise infectivity levels, if randomly generated strings are supposed to be ultra-ultra-ultra unlikely to ever find the function of interest. If that is so, if the functions of interest are so unfathomably rare that a random process could never be rationally expected to find the function, then why did they do so anyway?.
Whether the function is AS GOOD as the wild-type function is irrelevant. The function was found with a small pool of randomly generated peptides. Why? Why was this result possible if, as IDcreationists argue, the function is “hyperastronomically” rare in sequence space?
There are two papers dealing essentially with the same experiment. In the first experiment, they used a population size of ten initial sequences, and 7 rounds of mutagenesis and selection for increased infectivity, and with this achieved a meager 240-fold increase in infectivity.
They later publish another paper where they increase the population size to (IIRC) initially thousands, then later about a million, and with 20 rounds of mutation and selection achieve a ~17.000-fold increase in infectivity.
First paper:
Hayashi Y et. al. 2003.: Can an arbitrary sequence evolve towards acquiring a biological function? J Mol Evol. 2003 Feb;56(2):162-8. [DOI: 10.1007/s00239-002-2389-y]
Second paper:
Hayashi Y et. al. 2006.: Experimental rugged fitness landscape in protein sequence space. PLoS One. 2006 Dec 20;1:e96. [DOI: 10.1371/journal.pone.0000096]
Interestingly, the protein they evolve does not at all seem to approach the sequence of the wild-type protein. Implying it is either an entirely different hill in the sequence space, or possibly that the hill with the function is so broad that sequences occupying it can be entirely dissimilar.
There are at least three.
I haven’t read any, no matter how many there might be.
hear. hear.
Should I follow the thread there, the thread here, or try to do both at once.
No, that is not the ID argument.
Can’t we all at least agree that the truth matters?
Yet, the IDiots wonder why they fail to convince us that “only design makes sense,” when we watch them irrationally pronouncing against any results that go against their prejudices. Sorry, but an IDiot’s irrationality neither magically translates into the impossibility of evolution, nor into the existence of a magical being in the sky.
It’s the fallacy underlying all the reasoning with regards to the evolution of complexity, a particular species in our biosphere, the bacterial flagellum, other proteins and so on.
Entropy,
His argument has nothing to do with exploring sequence space. 500 bits of functional information is an indicator of design. If an amino acid change causes purifying selection then that amino acid is important to the organisms function.
His foot is fine:-))
What is problematic to your position is that a wild type exists in nature. Where did it come from?
Also this experiment is where 25% of the amino acids of the enzyme were changed. The change was in a row, but 25%.
You said something different then gpuccio’s argument thus a straw-man. You are interpreting what he said versus really understanding his position.
This statement means that random change did not find the wild type and in addition the sequence was very different. This is very significant to his position and does not require your straw-man to make it valid.
Again, how do you explain the origin of the wild type?
I would recommend re-reading the 2014 thread.
You even “participated”.
No it doesn’t, at all. The fact that a random sequence did not mutate towards the wild-type under selection for the same function (infectivity), does not mean that the wild-type did not or could not have evolved in the same way; from some arbitrary location in sequence space under selection for infectivity.
It simply doesn’t follow.
The experiment shows that the function can evolve from an arbitrary position in sequence space.
How is that any less of a problem for your position? Are you asking that question because you believe you really know the answer? Lemme guess: It was poofed into existence with godmagic?
Yes, that isn’t a subject of contention here.
But “It is under purifying selection” =/= “It exists nowhere else in sequence space”. For all we know, there could be a hill with a similar function in the immediate vicinity, with a narrow but deep fitness valley (wrt to ATPase/ATP synthase function= separating the other hill from the existing one. You can’t actually know that this isn’t the case without empirically exploring that surrounding space.
The detection of purifying selection for a particular function can at most indicate that there is a hill surrounded by fitness valleys for that function. It does not say ANYTHING about the density by which hills with similar functions exist in sequence space.
But interestingly, what we know from the existance of the P-loop NTPase superfamily is that, while it might be the case that the ATPase/ATP synthase function is surrounded by a fitness valley, it is also surrounded by hills constituting other functions.
Rumraket,
The statement forced you into speculation and away from evidence.
Again, the experiment did not find the wild type. That appears to be a fact. Your follow on statement
is false as the experiment did not find the wild type which is 2000 times more potent then the enzyme found by experiment.
Rumraket,
I will post this at UD prior to making any comment.
Good thing you didn’t say I contributed. 🙂
No, the statement made me correct your error in reasoning. But in order to correct that error in reasoning, I have to show that there are other logical possibilites you can’t rule out without doing an empirical enquiry. An emprical enquiry you haven’t actually done. And the experiment didn’t do.
You are ruling out a case the experimental setup simply does not have the capacity to rule out. YOU are the one deriving a conclusion from mere speculation.
You THINK you are going by the results of the experiment, but you are ACTUALLY doing an unwarranted extrapolation.
The experiment did not seem to move towards the wild-type sequence. But we technically don’t know whether the wild-type and the experimental protein sit at local optima on opposite sides on a much broader hill with a rugged surface, or if they are actually separated by a nonfunctional valley that can’t be traversed without losing the infectivity function entirely.
Wrong again. My statement isn’t false. Think Bill, THINK.
Only a tiny portion of sequence space has been explored in this experiment. The whole experiment was started by a single random sequence at some arbitrary and random place in sequence space.
From that initial starting position, only a few million steps away from the starting position were probed. And not in a line, but in many many thousands of directions, meaning the total distance from the starting position, if measured in a line, is only about 50 mutations in total.
But sequence space is vast, incredibly vast. I know you know this, you speak about how huge it is all the time. So please think for a moment Bill. How big a fraction of sequence space was probed by those few million steps? An infinitesimally tiny fraction. The experiment did not end up all that far away from the starting sequence. In fact the final protein they evolved had only about 30 substitutions, of which only one fixed the same amino acid as present in the same location in the wild-type.
Suppose the experiment was started from an entirely different location in sequence space. Suppose it had started at a location 10^20 permutations away. As in from another random place with an entirely different starting sequence that had 0 similarity to the one they happened to use.
Would that new location much further away, have allowed movement towards the wild type? Or is there a third hill, again with a similar function? We don’t know. I don’t know, you don’t know, nobody knows. But SINCE WE DON’T KNOW, you can’t then CLAIM to know that the wild-type, or a sequence with an infectivity level LIKE the wild-type COULD NOT have been reached from some OTHER place in sequence space. You don’t know whether there are other hills out there, and you don’t know how tall they are if they exist.
When you claim the wild-type could NOT have evolved from a random starting position by probing a few million alternative versions, simply because it didn’t happen from this ONE spot in sequence space, you are effectively claiming to know that there is no random place in the sequence space from which the wild-type, or similar levels of infectivity, can be reached. How do you know that? You don’t, that can’t be known without doing the actual exploration.
And in any case, you are still left having to explain why the infectivity function was found among 10 random starting clones. If the infectivity function is ultra-rare, then why was it found among 10 random starting clones?
Quite the contrary. It is the materialists with their fallacy of simplicity that are the misguided ones.
It must have been simple enough at the beginning for it to have occurred by blind dumb luck. There’s no evidence for it, of course. But the evidence just doesn’t matter.
Hey, I was frequently told it’s not about winning. “We’re just playing”. xD
Bill,
Come on man, you’re better than that. At least you’ve convinced me that you’re better than that. What about you re-read for comprehension?
Of course it does: how did he “measure” those increments in bits Bill? Did he make a blast comparison? Yes. Did he assume that any conserved pieces between human protein and whatever-else protein is functionally important? Yes. How did he justify this assumption? By claiming that since the time of separation between the lineages, all of the unimportant positions would have already changed.
I repeated the bolded part a zillion times before, yet you insisted on missing it. So, here it goes again: what does that mean? I can tell you: it means that gpuccio thinks that there was enough mutations to erase all unimportant sites and leave as identical only the ones related to function. Now pay close attention: If that’s true, then there was quite a bit of sequence-space exploration. Of course, gpuccio didn’t notice this, but he shot himself in the foot.
Before answering, please check what I’m saying, because you’re missing it again, and again, and again, and again, and I’m losing my patience. I’d like to keep it amicable between you and me. I’d really like that, but you seem to want it otherwise. It is very impolite to pretend to understand, only to show that you didn’t get it (or that maybe you don’t really care about those explanations). So, if you really don’t care, please tell me so, and I’ll stop trying to explain this to you.
Only if you think that gruyere is a good look for a foot.
I understand his position very well.
You’re making my point without realizing it, which means that you’re not understanding what I wrote. The only way in which that part would be very significant for his position is if he thinks that only finding the wild type sequence will do, which is precisely the problem I mentioned and you called a straw-man. He thinks that the only solution is the one that has been sequenced from wild type phage. I say there’s plenty of solutions and we just happen to know of the ones that prevailed and that we have sequenced.
As the solution that happened to be “found” through the evolutionary history of that phage.
There is no such thing as a fallacy of simplicity. It follows immediately by basic principles of probability, that simplicity is more likely than complexity. In so far as X was possibly generated at random, X was more likely to occur if X is simple, than if X is complex. If this isn’t immediately obvious to you, then we should be having an entirely different discussion that would have to start with you taking all of elementary school over again.
I have never seen anyone actually engage in that specific type of reasoning. Rather, what reasoning has been engaged in is simply that simpler things would be more likely to occur than more complex things.
Also, there is no actual level of complexity that would make it impossible to occur by blind dumb luck. The more complex it is, the more infrequent it would become over some timescale, but at no point does it cross over from just more infrequent on average, to actually impossible.
The only thing you could ever really derive, at least by reasoning alone, from a complex beginning, would be that the average frequency of occurrence of similar beginnings would be proportionally low. You would technically never be able to say that it couldn’t possibly happen at all.
Ironically there is no evidence for design, and there IS evidence for more simplicity the further we go back in time. Just look at the tree of life.
Yes, materialists will always be able to fall back on, “it just happened, that’s all. No reason. Jusrt sheer dumb luck.” The absolute of irrationality.
Why don’t people just get brutally honest with gpuccio and let him know that no matter how improbable something may be, that just doesn’t matter.
If they will always be able to fall back on it, then you are effectively conceding that the logic is valid. So it can’t be irrational.
Q.E.D.
What if it did? I mean, I’m sure you wouldn’t all be screaming “teleology!” “targeted evolution proven!” right?
It does matter, but the problem is Gpuccio is leaving out the probability of design.
A design hypothesis has to explain why X happened as opposed to Y, and give a probability of X on design.
That whole thing is simply skipped by design proponents. The calculation is attempted for a “blind material process”(and for some reason it’s always assumed to be like a tornado in a junk yard), but no calculation is attempted for design.
If explanation A is preferred to explanation B because B is unlikely, it has to be shown that A is more likely than B. This is just blindly assumed by design proponents.
What is the probability that deities in general make living organisms by using the F and V-type ATPase molecules known to exist? No number is given, or estimated, or even thought of. It is just assumed to be 1.
There is no hypothesis of design that says why anything is the way it is. It’s all just ad-hoc reasoning. Well, an omnipotent God could have done it, so since it could have done so, we’ll just assume it wanted to. It’s unfalsifiable nonsense.
Scientists are actually trying to figure out how life originated, nobody is intellectually satisfied with just saying “chance did it”, even if we can conceptually accept that chance “could” do it. But we want to know the how and the why. We want an explanation, not just a label.
Chance is a sort of null-hypothesis that can be rejected by showing that the evidence is more likely given a particular hypothesis. But a hypothesis implies a mechanism with explanatory power and scope. Something that explains why the data is a certain way. The problem with the design-rationalization is it can be mindlessly invoked to explain everything. It predicts nothing in particular, but can be brought up in ad-hoc fashion to “account” for any conceivable observation as “what the designer wanted”.
It’s like they’ve mistaken the Heart Of Gold, the infinite improbability drive, for their designer.
Entropy,
I have my better days:-)
Yes and no. You generally get his methods. He realizes this is not a direct measurement and indirect measurements have limitations. He has specifically defined all this. At this time I have not seen a better measurement of functional information.
I will have to use that one:-)
I disagree here. I will post this at UD and check with him before I comment.
Did you read how many trials Hayashi thought he needed to find this sequence?
Quoting Dave here as it’s relevant to this topic
Abstract
How new functions arise de novo is a fundamental question in evolution. We studied de novo evolution of promoters in Escherichia coli by replacing the lac promoter with various random sequences of the same size (~100 bp) and evolving the cells in the presence of lactose. We find that ~60% of random sequences can evolve expression comparable to the wild-type with only one mutation, and that ~10% of random sequences can serve as active promoters even without evolution. Such a short mutational distance between random sequences and active promoters may improve the evolvability, yet may also lead to accidental promoters inside genes that interfere with normal expression. Indeed, our bioinformatic analyses indicate that E. coli was under selection to reduce accidental promoters inside genes by avoiding promoter-like sequences. We suggest that a low threshold for functionality balanced by selection against undesired targets can increase the evolvability by making new beneficial features more accessible.
Fascinating. That paper supports all the reasons I gave in my earlier post where I tried to explain why the infectivity function exhibited by the random protein in the Hayashi et al papers, evolved so easily. Binding interactions between molecules are ubiquitous. Things sticking together at the molecular level is pervasive and almost unavoidable.
Unfortunately E-Coli didn’t turn into possums or giraffes, so evolution fails again. This is it guys. It’s over. Sad but true
I absolutely get his “methods.” I get his assumptions and “justifications” too. Here from the horse’s mouth (interestingly from a comment directed at you). Emphasis mine:
So, if this is true, then there has been quite a bit of exploration of sequence space. A shot directly to his own foot. Since you think that’s the best method to measure “functional” information, and since it implies quite a comprehensive evolutionary exploration of sequence space what should we conclude?
As if the guy was capable of giving an honest answer.
Not the wild type sequence Bill, not the wild type sequence, but activity comparable to the wild type. Very different things. In evolutionary experiments we don’t expect to find the wild type sequences.
I saw how many particles they estimated to need in order to attain activity comparable to wild-type. I also noticed that they mentioned limitations to the experimental setting, which I had already noticed. So I’m not sure why I should worry about any of that.
You seem to be missing the importance of the result. They found new solutions to infectivity, and the infectivity evolved from random peptide libraries under limited conditions.
It doesn’t matter if gpuccio, or anybody else, hand-waves at the results. I can see their potential, because I neither have irrational expectations from the experiments, nor do I have a commitment to some magical being in the sky. So I take the results as they are, rather than wishing they didn’t happen, and feeling threatened by them to the point of holding to anything, even misconceptions about what the experiments should produce, in order to reject them altogether.
I want to understand how things work. These experiments help me do just that. Again, they confirmed two of my suspicions, that there’s more than one solution to a problem, and that even point mutations can measurably improve an activity when starting with random peptides.
As you see, my take is rational, and doesn’t require me to hold to a philosophically faulty position such as designers designing designers, cherry-picking “design” while ignoring all that’s required before we can even talk about design (cart-before-the-horse), etc.
😩
Why must design proponents give reasons and explanations when materialists don’t have to give reasons and explanations?
It’s irrational because it is
1. without the faculty of reason; deprived of reason.
2. without or deprived of normal mental clarity or sound judgment.
3. not in accordance with reason; utterly illogical: irrational arguments.
4. not endowed with the faculty of reason:
They must both give reasons and explanation. The problem is that it is the IDcreationists who skip that part every time. There is still no theory of ID. It’s all negative arguments against tornadoes in junkyards, there is no explanatory theory of ID for ANY biological entity.
For evolutionary biology, reasons and explanations is built on the basis of data from geology, paleontology and comparative genetics. Data from these fields are used to construct hypotheses about what happened, which are then tested against new data and by seeing how well different models can explain already collected data. There are mechanisms such as mutations, and forces affecting gene frequencies such as natural selection.
What does ID have? Endless bullshit about tornadoes in junkyards being unlikely to do X, so “design” mustadunit. But we’re never actually shown that design is more likely than the tornado to do X. That’s just implicitly assumed. An intelligent designer could do it. Perhaps, but what are the odds that it would? Chance also could do it, but at least we get estimates at a number. If I am to compare scientific hypothesis on account how likely they are to account for X, I’m going to need numbers for both so I can pick the more likely option.
If IDcreationists can always just assume that their designer would make X, then I could just as well always assume that the conditions happened to be just right for the tornado to make X.
It is fantastically ironic that ID proponents are essentially guilty of the very thing they are (usually falsely) accusing evolutionary biologists of.
gpuccio @ UD,
He has me there. Can anyone think of a process whereby something can be optimised by trial and error?
Also can anyone think why sequences that do less have been replaced by those that do more to the degree that we only see the “tips” of the branches now, and not the incremental sequences leading up to the extant ones?
Bueller? Bueller? Oh, wait, he’s an IDiot too!
gpuccio non-ironically:
It’s funny then how design never seems to explain anything other then why evolution could not do it.
It’s not an explanation in any sense of the word. It could have been Zeus or my grandma. There’s literally no way to rule any cause in or out.
What, the word “Design” explains it does it? As that’s all I can see.
Still blathering on about the level of infectivity, rather than seriously engaging the huge issue that the very first sequence used to replace the wild-type domain, had the desired function already at a level that natural selection could operate on.
The level of infectivity you can obtain in 35 substitutions from where you start out, obviously depends on where in sequence space you start out. If you are far from peaks with wild-type levels of infectivity, it will take more substitutions, or more random starting positions. How is this a surprise or a problem?
What the hell is he talking about? A big hole? But okay, he concedes the central point. The function is ubiquitous in sequence space and easy to find.
Has anyone tried a similar experiment with recombination? I don’t know if that’s even possible, just curious since I remember Pitr pointing out that was a limitation of the technique used there
That would certainly make the ability to jump around large distances in sequence space a reality, and it might be how the wild-type sequence evolved.
But, I don’t believe it was. Searching uniprot for dissimilar but related sequences to the D2 domain, gives thousands of hits, and there seem to be a very large span of sequence identities going from 98% similarity all the way down to 18% in initial results. From 59% identity down to 18% identity I’m finding several hundred similar sequences that gradually diverge from the g3p D2 domain, in half-percentage increments. That implies the sequence has been evolving incrementally by point mutations over many hundreds of millions of years, from some totally different sequence.
It’s not that the current sequence was suddenly magicked up by mutations, we are probably talking of an arms race between an infectious phage, and bacterial hosts constantly evolving away from it. Meaning surface proteins on bacterial hosts constantly forced to change because they’re preyed upon by phages, which are forced to constantly change and adapt to the host.
Entropy,
You can destroy homology by searching a tiny fraction of the sequence space. If you read his comments you will see that he realizes that only a tiny fraction of the search space has been explored. The evidence in his favor is the preservation of the sequence. As Rumraket says this is not proof positive because local optimas may be next to each other. All the evidence is not in but it appears to be favoring his hypothesis.
gpuccio:
OMagain:
Heh.
Sorry, that doesn’t work. In order for the synonymous substitutions to be saturated the mutations must be at such point that the software can no longer estimate how many mutations there’s been. In order to touch each and every position the sequence would have to have suffered quite a chunk of mutations. No way around.
Do you really think I missed that? He’s contradicting himself and he doesn’t even notice! He presented that shit about the maximum that he thinks evolution would explore, and even talks about the impossibility to touch every position in a genomic sequence in the OP and the comments section. But here, he says that he can measure “jumps” in “functional” information because there’s been enough time to touch every position in the sequence. Go figure.
For the preservation to be a measure of important sites, he needs the sequence to have mutated enough to touch every position. He even claims that to be the case. That means a lot of exploration of sequence space. Read his explanation.
I truly cannot believe that you don’t see the problem. It’s painfully obvious.
Since the problem is so painfully obvious I’m starting to doubt I’m writing in English.
Entropy,
You can touch every position in 500-5000 mutations. The entire search space is 20^500. I am sure you know this I am just trying to communicate.
Lets just agree that he has come up with an indirect method to measure functional information in proteins. At this point it is a relative measure.
He may have contradicted himself from time to time as we all have.
His work is interesting to me as it shows genetic information change over time, and his posts are always educational.
Definitely not. Just for E coli (one of the examples he used in that “evolution cannot do it” OP), there’s 4 million bases. About 4000 genes. There’s no way you can touch every position with 500-5000 mutations. Let alone to the point of saturating all the synonymous positions. Saturating Bill. That’s the word gpuccio himself used. Saturation. For that you need a number of mutations well beyond the number of bases. That means quite a bit of “bits” available for evolution.
A method that depends on evolution having explored a huge amount of sequence space.
The problem being that here he’s contradicting himself to the point of defeating his own position. He has contradicted himself in a very profound way. But don’t worry. Nobody will notice. You won’t notice after I explained this several times over. Given that, nobody on his side will. It’s just impossible for you guys to notice such profound mistakes. You lack something. I don’t know what. But something important. I’ll be forever amazed at this.
So, it doesn’t matter, to you, that the method depends on evolution being able to explore quite a bit of sequence space?
“Design,” of course, is a category of causes, not a cause itself. I still think one could conclude that design was responsible for something or for some things without knowing exactly what or who caused it, but it would have to fit the category of design causes. Notably, some sort of rational knowledge that breaks through the limits of “natural processes” (like evolution) would need to be in evidence. The stupid “evolution can’t do it” is a sort of attempt to come up with something like that, they just forget that they need an intelligent cause that transcends evolution, not just find some lack in the current explanatory processes. They assume that intelligence did it because they are generally contemptuous of any process of discovery that doesn’t consider an undefined Designer as a live option in science–because they’re religious, not scientific, in orientation.
Because God can do anything, in their view.
Yes, there’s nothing at all in “nature” that they’ve managed to actually identify as having been designed.
Glen Davidson
In GPuccio’s OP “Bioinformatics tools used in my OPs: some basic information” https://uncommondescent.com/intelligent-design/bioinformatics-tools-used-in-my-ops-some-basic-information/ , he explains his method.
At one point I posted about a huge information jump https://uncommondescent.com/intelligent-design/bioinformatics-tools-used-in-my-ops-some-basic-information/#comment-644097 involving thousands of unexplained bits.
In his response GPuccio explained me why this cannot be used, or rather why he chooses not to use the mammal transition. His reasons are rather subtle. I think that his explanation is relevant to some of the objections here:
The key remark is this “That mean that what is conserved after that time is certainly conserved because of functional constraint.” IOWs sequences which are conserved over such a long time are functional beyond any doubt.